Causal Inferences

Estimating how much an intervention helps a given individual the conditional average treatment effect (CATE) is increasingly central to decision-making in medicine, economics, and policy, where an estimate is most useful when accompanied by a calibrated uncertainty interval. We study the few-placebo regime, in which one treatment arm is much smaller than the other, as arises in unequal-allocation trials and small-holdout $A/B$ tests. The standard estimator in this setting is the X-Learner, and a natural way to obtain credible intervals is to make its second stage Bayesian. We show that these intervals under-cover: they contain the true effect less often than their nominal level. We trace this to a structural cause the X-Learner's regression target inherits the bias of a nuisance model fitted to the small arm, so the posterior is centered away from the true effect and we find that the standard remedy, regressing an orthogonal doubly-robust score, is also unreliable here, since the regime's limited overlap leaves the estimator either highly variable or, once stabilized, biased once more. Both consequences reflect a pattern that extends beyond causal inference: a separately estimated variance is attached to a point estimate of a hard-to-learn quantity, and the point estimate's bias is not captured by that variance. We propose GP-CATE, which models each arm's outcome surface with a Gaussian process, so the scarce arm's uncertainty enters the posterior directly rather than as an unmodelled bias. Across synthetic and semi-synthetic benchmarks, GP-CATE attains calibrated coverage where the estimators we compare against including Causal Forest and BART do not, at the cost of intervals that are appropriately wide when the data are uninformative.

Automated prompt optimization methods (e.g., DSpy, TextGrad) can substantially improve the performance of large language model (LLM), however, their generalization ability across different tasks remains underperformed. In practice, the superiority of the optimized prompt on one benchmark often fails to transfer to another, and this limitation persists even when switching across different LLM backbones. To investigate the underexplored sources of heterogeneity in prompt performance, we conduct a causal inference-inspired observational analysis of optimized prompts across a diverse set of optimization frameworks, LLM backbones, and NLP benchmarks. To achieve the goal, we build upon the propensity-adjusted associational analysis together with multiple complementary representations of prompt edits, where the consistent task-conditioned edits patterns are identified. We find that complexity-increasing and meta-instructional edits are negatively associated with mathematical and multi-hop reasoning performance, whereas step-by-step and meta-cognitive edits improve logical and sequential reasoning tasks. These effects are robust across cognitive-load annotations, surface-level text features, and edit-motif analyses, and can generalize across optimization frameworks. Overall, these results indicate that prompt optimization failures arise from systematic interactions between edit families and task characteristics rather than random optimization artifacts, providing feature-level characterization of optimizer behavior and motivating future task-conditioned optimizer design.

Understanding the effects of interventions is central to scientific progress, with randomized controlled trials (RCTs) regarded as the gold standard for causal inference in many applied fields. However, RCTs are costly, time-consuming, and often constrained by ethical or practical limitations, motivating the need for causal methods able to draw conclusions from observational data. While such data is collected at ever larger scale, making its use for causal inference is often hindered by the fact that not all variables affecting treatment allocation and the outcome are observed: an issue known as unobserved confounding. In this paper, we introduce a new study design called confounder detection via treatment intent. The idea is to query a human expert who makes treatment decisions, and ask them to compare pairs of units proposed by a principled matching strategy, with the goal of eliciting unobserved variables that explain why treatment decisions differ. We provide a theoretical basis for such a procedure, ascertaining conditions under which such a study design may elicit unobserved confounders. Building on this newly established foundations, we study treatment effects of interventions in the intensive care unit (ICU). First, we show empirical evidence strongly indicating that electronic health records (EHRs) collected in ICUs are subject to unobserved confounding. By using clinical text notes as a proxy for physicians' knowledge and leveraging natural language processing, we provide a proof of concept for our methodology in a semi-synthetic environment with a known ground truth.

Large language model (LLM) development is currently driven by large-scale empirical iteration over data mixtures, reward models, routing strategies, and evaluation pipelines. Here, we argue that many central questions in LLM development and evaluation are inherently causal: What is the effect of adding a data domain during pretraining? How do annotator preferences change when LLMs generate text in a different style? Should a prompt be routed to a larger or smaller model given inference cost constraints? In general, causal methods are well-suited to such settings where interventions change outcomes but, surprisingly, are underrepresented in LLM development. Our contribution is threefold: (1) We explain how causal methods can help develop modern LLM development and evaluation: LLM development relies heavily on logged data, which are often subject to confounding and distribution shifts; evaluation uses learned but potentially biased judges; and deployment environments are non-stationary. These conditions make purely predictive approaches fragile and create opportunities for principled identification and estimation methods from causal inference. (2) We further map opportunities for causal methods in the entire LLM development pipeline, including pretraining, alignment, routing, agentic workflows, and evaluation. (3) We discuss new research opportunities around leveraging causal methods for LLM development and evaluation. Overall, we argue that causal methods are potentially underutilized for the LLM development and evaluation pipeline, despite the fact that such methods can ensure a reliable and scientifically grounded design.

We study counterfactual distribution learning for high-dimensional outcomes whose counterfactual law may concentrate near lower-dimensional structure. Standard isotropic smoothing treats all ambient directions equally, leading to unfavorable scaling and unstable local inference. We propose two diffusion-guided estimators based on semiparametric debiasing: diffusion-informed smoothing for counterfactual densities and diffusion-informed score smoothing for counterfactual scores. The estimators combine causal nuisance adjustment with geometry-adaptive localization driven by diffusion score information, removing first-order nuisance bias while aligning smoothing with local outcome geometry. We establish asymptotic expansions, risk bounds, and inference procedures for smoothed density and score-based targets, with ambient density inference obtained under additional approximation conditions. Under structural geometry conditions, the leading stochastic error is governed by an effective dimension induced by the diffusion-guided kernel, rather than by the ambient dimension. Semi-synthetic experiments based on CelebA show steeper error decay for geometry-adaptive methods, supporting the proposed effective-dimension theory.

Modern Artificial Intelligence achieves remarkable predictive power by optimizing statistical risk functionals over vast corpora. Yet a gap separates this from genuine intelligence: the inability to distinguish correlation from causation. This paper argues that causal inference (identifying mechanisms invariant under intervention) is AI's indispensable statistical conscience. Without causal grounding, AI systems are correlation machines: powerful in familiar domains, brittle under distribution shift, and biased in high-stakes settings. Three contributions develop this argument. First, a Statistical Necessity Theorem for Causal Generalization: any algorithm achieving out-of-distribution generalization must encode causal structure, formalizing the distinction between prediction P(Y|X) and intelligence P(Y|do(X)). Second, a unified framework connects Pearl's do-calculus, the Potential Outcomes framework, Double Machine Learning, and Invariant Risk Minimization as a family of Causal Statistical Estimators, each identifying interventional distributions under different assumptions. Third, three AI failure modes (hallucination in large language models, reward hacking in reinforcement learning from human feedback, and degradation under distribution shift) are manifestations of causal blindness, each admitting a principled statistical remedy. Trustworthy AI is, at its core, a problem of causal statistics. The statistical community is not merely equipped to solve it -- it is the only community with the foundational tools to do so rigorously.

Objective: The growing availability of large-scale observational clinical datasets and challenges in conducting randomized controlled trials have spurred enthusiasm in using causal machine learning (ML) for causal inference in observational data. We present a roadmap for applying causal ML to observational data. Materials and methods: We outline the importance of assessing validity assumptions within available data and applying causal ML responsibly for clinical experts using causal ML and ML practitioners with limited clinical expertise. Observations: Despite advances in causal ML, its limitations remain largely under-appreciated across disciplines. This gap in shared knowledge may impact the validity of findings. Discussion: Causal assumptions must be satisfied and modeling choices justified. Otherwise, these approaches risk producing biased or misleading results, with consequences for clinical research and patient care. Conclusion: Causal ML can be a powerful tool for generating causal hypotheses. We provide a template to strengthen the rigor and interpretability of causal analyses.

This work addresses the problem of learning directed acyclic graphs (DAGs) from nodal observations generated by a linear structural equation model. DAG learning is a central task in signal processing, machine learning, and causal inference, but it remains challenging because acyclicity is a global combinatorial property. Continuous acyclicity constraints have led to important algorithmic advances by replacing the discrete DAG constraint with smooth equality constraints. However, existing formulations still involve difficult non-convex optimization landscapes and may suffer from degenerate first-order optimality conditions. Here, we restrict attention to DAGs with non-negative edge weights and exploit this additional structure to obtain a simpler characterization of acyclicity. Building on this characterization, we formulate a regularized non-negative DAG learning problem and develop an algorithm based on the method of multipliers. We further analyze the benign optimization landscape induced by non-negativity. In the population regime, we show that the true DAG is the unique global minimizer of the proposed augmented-Lagrangian formulation; moreover, the landscape contains no spurious interior stationary points, and the true DAG is the only acyclic KKT point. Numerical experiments on synthetic and real-world data show that the proposed method improves over state-of-the-art continuous DAG-learning alternatives.

Conventional treatment policies map patient covariates to a single recommended intervention in order to maximize expected clinical outcomes. Although a rich body of causal inference methods has been developed to estimate such policies, point-valued recommendations can be highly sensitive to estimation uncertainty, model specification, and finite-sample variability, while typically providing little guidance about how confident one should be in the recommended action. In this work, we propose a set-valued policy learning paradigm for the multiple-treatment setting, in which policies output a set of plausible treatments rather than a single recommendation. This formulation enables intrinsic uncertainty quantification, with the size of the predicted set reflecting the degree of decision ambiguity. We extend the learning-to-defer framework to multiple treatments via a novel \textit{greatest Lower Bound} method, and introduce \textit{conformal policy learning}, which bridges the gap between unobserved ground-truth optimal treatments and estimated optimal treatment rules. Drawing on insights from the noisy-label literature, we develop a randomness-injection approach that guarantees marginal coverage without requiring assumptions on underlying black-box optimal treatment rules. Through experiments on synthetic data and a real-world application to In-Vitro Fertilization (IVF), we demonstrate that our methods produce robust and actionable policies that naturally incorporate clinical considerations while effectively balancing performance and reliability.

Individualized treatment selection with continuous actions requires accurate causal response estimation in decision-relevant regions, rather than uniformly over the entire action space. Estimating a global causal response surface and then choosing the treatment that maximizes it can therefore be suboptimal, since standard estimation objectives allocate modeling effort according to the observed treatment distribution rather than the regions that determine the optimal decision. While decision-aware approaches have been studied in unconfounded settings, this problem remains underexplored in proximal causal inference, where proxy variables and bridge functions enable identification under suitable assumptions even in the presence of hidden confounding. Despite recent progress, proximal methods have primarily focused on treatment-effect and potential-outcome estimation rather than treatment selection and optimal decision-making. To bridge this gap, we introduce a policy-targeted weighted bridge loss that emphasizes decision-relevant treatment regions while retaining global stabilization. We prove a regret bound showing that the proposed weighted bridge loss controls treatment-selection regret through a weighted ill-posedness constant. We instantiate the framework in decision-aware variants of several proximal bridge solvers, yielding practical algorithms that alternate between weighted bridge estimation, response-surface projection, policy update, and weight refinement. Empirically, we find that decision-aware weighting reduces regret across several bridge solvers, suggesting improved treatment selection in proximal settings.

Causal inference, estimating causal effects from observational data, is a fundamental tool in many disciplines. Of particular importance across a variety of domains is the continuous treatment setting, where the variable of intervention has a continuous range. This setting is far less explored and represents a substantial shift from the binary treatment setting, with models needing to represent effects across a continuum of treatment values. In this paper, we present the first causal foundation model for the continuous treatment setting. Our model meta-learns the ability to predict causal effects across a wide variety of unseen tasks without additional training or fine-tuning. First, we design a novel prior over data-generating processes with continuous treatment variables in order to generate a rich causal training corpus. We then train a transformer to reconstruct individual treatment-response curves given only observational data, leveraging in-context learning to amortize expensive Bayesian posterior inference. Our model achieves state-of-the-art performance on individual treatment-response curve reconstruction tasks compared to causal models which are trained specifically for those tasks. Inference code (including trained model weights) can be found at https://github.com/layer6ai-labs/CCPFN-inference .

Comparative evaluation of multiple dynamic treatment policies is essential for healthcare and policy decisions, yet conventional longitudinal causal inference methods estimate each in isolation, preventing information sharing across counterfactuals. We demonstrate that this separate estimation paradigm induces a structurally uncontrolled second-order bias, inflating finite-sample variance even after standard debiasing with longitudinal targeted maximum likelihood estimation(LTMLE). To address this, we propose a policy-aware reparameterization of Iterative Conditional Expectation (ICE) Q-functions that enables joint estimation through shared representations. We implement this approach in the Policy-Encoded Q Network (PEQ-Net), an architecture centered on a shared policy encoder. The encoder is trained using kernel mean embeddings, ensuring that the learned representation space reflects population-level policy dissimilarities. After applying an LTMLE correction step, we prove this design imposes a structural constraint on the second-order remainder, thereby stabilizing finite-sample variance. Experiments on semi-synthetic datasets demonstrate that PEQ-Net consistently outperforms existing ICE-based methods, achieving substantial reductions in root-mean-square error, particularly when evaluating closely related policies.

The instrumental-variables (IV) setting is standard for partial identification of causal effects when unobserved confounding makes point identification impossible. Existing approaches face methodological bottlenecks: closed-form bound estimands are required -- e.g., Balke-Pearl equations in binary IV -- and even when available, designing accurate estimators requires manual effort tailored to each estimand. While direct Bayesian inference of the causal effects, instead of the bounds, circumvents these challenges, it is often computationally intensive and suffers from high prior sensitivity or under-dispersed posteriors. As a remedy, we introduce IV-ICL, an amortized Bayesian in-context learning method that learns the marginal posterior distribution of the causal effects directly and derives bounds as its quantiles. Unlike standard variational inference that optimizes exclusive KL divergence, amortized Bayesian inference minimizes the expected inclusive KL, a mass-covering objective. We empirically observe that optimizing inclusive KL can recover the entire identified set across diverse data-generating processes, while exclusive-KL (e.g. with variational inference) of the same Bayesian formulation collapses onto a single mode and fails to cover the identified set. We evaluate IV-ICL on synthetic and semi-synthetic IV benchmarks and show it produces intervals that are more reliably valid and more informative compared to efficient semi-parametric, Bayesian, and plug-in baselines, at 20-500x lower inference time. Beyond methodology, we propose a procedure to convert randomized controlled trials into IV benchmarks with provably preserved ground-truth causal effects that enables a more realistic evaluation of partial-identification methods.

Trajectory-based data attribution methods estimate the influence of training samples on model predictions by unrolling the training trajectory. They are widely used in applications such as data selection, data valuation, and model diagnosis, but there is a lack of comprehensive error analysis of these methods, raising concerns about method faithfulness and hindering reliable deployment. In this work, we provide the first systematic analysis of error sources in trajectory-based data attribution, together with concrete remedies to mitigate them and practical guidelines for downstream use. We organize the total error into three categories, config-level, algorithm-level, and system-level. We make three contributions. First, we identify optimizer mismatch as the dominant config-level error: existing methods derive their attribution under the assumption of SGD, even for models trained with the modern de facto optimizer AdamW. We propose AdamW-influence to fully account for AdamW's optimization dynamics, yielding improvements from 10% to over 300% in Spearman correlation between estimated and ground-truth influence across four settings spanning MLP, CNN, GPT-2, and Llama 3.2-1B. Second, we isolate the remaining algorithm-level error arising from the first-order Taylor approximation, identify the learning rate and trajectory length as factors governing the error magnitude, and derive a closed-form error proxy that can be evaluated along the original trajectory without retraining. Third, we translate these insights into practical guidelines for data selection by unifying offline and online strategies under a K-step look-ahead framework. Under this framework, online selection with a short horizon often matches or exceeds offline, and the optimal horizon can be tuned jointly with the learning rate. Together, these results turn the framework into an actionable selection recipe for practitioners.

Automated systems built on artificial intelligence (AI) are increasingly deployed across high-stakes domains, raising critical concerns about fairness and the perpetuation of demographic disparities that exist in the world. In this context, causal inference provides a principled framework for reasoning about fairness, as it links observed disparities to underlying mechanisms and aligns naturally with human intuition and legal notions of discrimination. Prior work on causal fairness primarily focuses on the standard machine learning setting, where a decision-maker constructs a single predictive mechanism $f_{\widehat Y}$ for an outcome variable $Y$, while inheriting the causal mechanisms of all other covariates from the real world. The generative AI setting, however, is markedly more complex: generative models can sample from arbitrary conditionals over any set of variables, implicitly constructing their own beliefs about all causal mechanisms rather than learning a single predictive function. This fundamental difference requires new developments in causal fairness methodology. We formalize the problem of causal fairness in generative AI and unify it with the standard ML setting under a common theoretical framework. We then derive new causal decomposition results that enable granular quantification of fairness impacts along both (a) different causal pathways and (b) the replacement of real-world mechanisms by the generative model's mechanisms. We establish identification conditions and introduce efficient estimators for causal quantities of interest, and demonstrate the value of our methodology by analyzing race and gender bias in large language models across different datasets.

In the data-driven era, large-scale datasets are routinely collected and analyzed using machine learning (ML) and artificial intelligence (AI) to inform decisions in high-stakes domains such as healthcare, employment, and criminal justice, raising concerns about the fairness behavior of these systems. Existing works in fair ML cover tasks such as bias detection, fair prediction, and fair decision-making, but largely focus on static settings. At the same time, fairness in temporal contexts, particularly survival/time-to-event (TTE) analysis, remains relatively underexplored, with current approaches to fair survival analysis adopting statistical fairness definitions, which, even with unlimited data, cannot disentangle the causal mechanisms that generate disparities. To address this gap, we develop a causal framework for fairness in TTE analysis, enabling the decomposition of disparities in survival into contributions from direct, indirect, and spurious pathways. This provides a human-understandable explanation of why disparities arise and how they evolve over time. Our non-parametric approach proceeds in four steps: (1) formalizing the necessary assumptions about censoring and lack of confounding using a graphical model; (2) recovering the conditional survival function given covariates; (3) applying the Causal Reduction Theorem to reframe the problem in a form amenable to causal pathway decomposition; (4) estimating the effects efficiently. Finally, our approach is used to analyze the temporal evolution of racial disparities in outcome after admission to an intensive care unit (ICU).

Causal sensitivity analysis aims to provide bounds for causal effect estimates in the presence of unobserved confounding. However, existing methods for causal sensitivity analysis are per-instance procedures, meaning that changes to the dataset, causal query, sensitivity level, or treatment require new computation. Here, we instead present an in-context learning approach. Specifically, we propose an amortized approach to causal sensitivity analysis based on prior-data fitted networks. A key challenge is that the sensitivity bounds are not directly available when sampling training data. To address this, we develop a general prior-data construction that is applicable across the class of generalized treatment sensitivity models. Our construction involves a Lagrangian scalarization of the objective to generate training labels for the bounds through a tradeoff between causal effect min/max-imization and sensitivity model violation, which avoids model-specific analytical derivations. We further show that, under standard convexity and linearity conditions, our objective recovers the full Pareto frontier of solutions. Empirically, we demonstrate our amortized approach across various datasets, causal queries, and sensitivity levels, where our approach achieves a test-time computation that is orders of magnitude faster than per-instance methods. To the best of our knowledge, ours is the first foundation model for in-context learning for causal sensitivity analysis.

In causal inference, confounders are variables that influence both treatment decisions and outcomes. However, unlike as in randomized clinical trials, the treatment assignment mechanism in observational studies is not known, and it is thus unclear which covariates act as confounders. Here, we aim to generate insight for causal inference and answer: which of the observed covariates act as confounders? We introduce ConfoundingSHAP, a Shapley-based method for attributing confounding strength to individual covariates. Our contributions are twofold. First, we propose a Shapley game targeted to infer the confounding strength of the covariates. Our resulting Shapley values differ from the standard applications of SHAP explanations on causal targets, such as understanding treatment effect heterogeneity, which are ill-suited for our task. Second, as our task requires evaluating the value function over many adjustment sets, we provide a scalable TabPFN-based estimation that avoids exhaustive refitting. We demonstrate the practical value across various datasets, where ConfoundingSHAP provides informative explanations of which observed covariates drive confounding and thereby helps to provide more insight for causal inference in practice.

Distributional causal inference requires estimating not only average treatment effects but also interventional outcome distributions, including quantiles, tail risks, and policy-dependent uncertainty. As a method for distributional causal inference, generative adversarial network (GAN)-based counterfactual methods are flexible tools for this task. However, these methods have several limitations. First, the objectives of certain techniques do not coincide with the statistical risk of the identifiable causal target, and therefore provide limited theoretical guarantees regarding estimable counterfactual distributions or optimality. Second, they tend to rely on unstable density-based methods, such as density ratio estimation. In this paper, we propose GANICE (GAN for Interventional Conditional Estimation) with several advantages: it (i) clarifies the conditional interventional distribution for each treatment--covariate state as the causal estimation target; (ii) estimates the conditional distribution such that its averaged Wasserstein risk is minimized; (iii) establishes minimax optimality. GANICE achieves these advantages through the introduction of the extended Wasserstein distance, the incorporation of a cellwise critic in its dual, and an optimality proof based on Besov space theory. Our experiments demonstrate that GANICE consistently outperforms existing methods.

Causal inference, especially in observational studies, relies on untestable assumptions about the true data-generating process. Sensitivity analysis helps us determine how robust our conclusions are when we alter these underlying assumptions. Existing frameworks for sensitivity analysis are concerned with worst-case changes in assumptions. In this work, we argue that using such pessimistic criteria can often become uninformative or lead to conclusions contradicting our prior knowledge about the world. To demonstrate this claim, we generalize the recent s-value framework (Gupta & Rothenhäusler, 2023) to estimate the sensitivity of three different common assumptions in causal inference. Empirically, we find that, indeed, worst-case conclusions about sensitivity can rely on unrealistic changes in the data-generating process. To overcome this, we extend the s-value framework with a new sensitivity analysis criterion: Bayesian Sensitivity Value (BSV), which computes the expected sensitivity of an estimate to assumption violations under priors constructed from real-world evidence. We use Monte Carlo approximations to estimate this quantity and illustrate its applicability in an observational study on the effect of diabetes treatments on weight loss.

Randomized controlled trials typically assume that prognostic covariates are known and available at no cost. In practice, obtaining high-dimensional pretreatment data is costly, forcing a trade-off between covariate-adaptive precision and a measurement budget. We introduce Dynamic Adaptive Rerandomization via Thompson Sampling (DARTS), which treats covariate acquisition as a sequential optimization problem embedded within a design-based causal inference task. A budgeted combinatorial Thompson sampler learns which covariates are most prognostic across successive batches; selected covariates then drive rerandomization and regression adjustment to reduce batch-level average treatment effect variance. Our primary theoretical contribution is a decoupling result: adaptive covariate selection based on past batches preserves batch-level randomization validity, and the cumulative inverse-variance weighted estimator achieves at least nominal asymptotic coverage. We further derive a Bayes risk bound for the acquisition layer that matches the minimax lower bound up to logarithmic factors. Empirically, DARTS systematically concentrates the budget on informative features, significantly closing the efficiency gap to oracle designs while maintaining strict inferential validity.

Multimodalpersonalityunderstandingplaysacriticalroleinhuman centered artificial intelligence. Previous work mainly focus on learn-ing rich multimodal representations for video personality under standing. However, they often suffer from potential harm caused by subject bias (e.g., observable age and unobservable mental states), as subjects originate from diverse demographic backgrounds. Learn ing such spurious associations between multimodal features and traits may lead to unfair personality understanding. In this work, weconstruct aStructural Causal Model (SCM)toanalyze theimpact of these biases from a causal perspective, and propose a novel Dual Causal Adjustment Network (DCAN) to mitigate the interference of subject attributes on personality understanding. Specifically, we design a Back-door Adjustment Causal Learning (BACL) module to block spurious correlations from observable demographic factors via a prototype-based confounder dictionary, and subsequently ap ply a Front-door Adjustment Causal Learning (FACL) module to ad dress latent and unobservable biases throughalearnedmediatordic tionary intervention, thereby achieving causal disentanglement of representations for deconfounded reasoning. Importantly, we con struct a Demographic-annotated Multimodal Student Personality (DMSP) dataset to support the analysis and discussion of fairness related factors. Extensive experiments on the benchmark dataset CFI-V2 and our DMSPdataset demonstrate that DCAN consistently improves prediction accuracy, reaching 92.11% and 92.90%, respec tively. Meanwhile, the improvementsinthefairnessmetricsofequal opportunity and demographic parity are 6.57% and 7.97% on CFI-V2, and 15.38% and 20.06% on the DMSP dataset. Our code and DMSP dataset are available at https://github.com/Sabrina-han/DCAN

In routine care, individuals identified a priori as high-risk are usually tested for conditions more frequently. Protected attributes, such as sex or ethnicity may also determine testing frequency. Such heterogeneous detection rates across a population induce label error. This causes systematic model error for specific groups and biases performance metrics during validation. This paper proposes a method to correct for such bias in prediction models due to differential diagnostic delay. We use a causal inference framework to define our target estimand: an individual's diagnosis probability in a counterfactual scenario where their diagnosis rate matches that of a reference group. We model the longitudinal process as a hidden Markov model, in which confirmatory test results are emissions from a latent progressive disease stage. We validate our approach in simulated data and apply it to a case study of chronic kidney disease prediction using electronic health records. In simulations, our method reduces prediction bias and improves calibration-in-the-large, correcting the Observed:Expected ratio in the underdiagnosed group from 1.34 (standard deviation: 0.09) in a model developed without any correction for underdiagnosis bias to 1.02 (0.09). Violations of assumptions in the simulation affected the estimation of model parameters, but the proposed approach nonetheless remained better calibrated than the standard model. In the clinical case study, we identify diabetes as the main driver of observability, with an odds ratio of 10.36 (95% confidence interval, 9.80 - 11.02) in 6-month urine albumin-creatinine ratio testing rate. Using our approach to predict the counterfactual diagnostic rate in patients without diabetes, we improved the Observed:Expected ratio of a developed clinical prediction model from 1.55 (1.51 - 1.59) to 1.01 (0.98 - 1.04).

Instrumental variable (IV) and control function (CF) methods are powerful tools for causal effect estimation in the presence of unmeasured confounding, yet most existing approaches target only mean effects and/or demand substantial fitting and tuning effort. In this paper, we introduce a simple method, TabCF, for control function regression using tabular foundation models, which enables accurate, fast, identification-transparent, and tuning-light causal estimation of distributional quantities, such as interventional means and quantiles; we also propose a copula-based approximation for multivariate outcomes. TabCF performs favorably against representative methods across a broad range of small- to medium-sized synthetic and real data scenarios. The central message is two-fold: for practitioners, it highlights that TabCF is an effective tool for distributional causal inference; for researchers, it suggests that the proposed approach could be considered a strong baseline for future method development. Code is available at https://github.com/GepingChen/TabCF.

Estimating causal effects from observational data has become increasingly critical in diverse fields including healthcare, economics, and social policy. The fundamental challenge in causal inference arises from the missing counterfactuals and the selection bias. Existing methods are largely limited to point estimates and lack the capacity for distribution modeling. In this work, we propose RepFlow, a novel framework that formulates causal effect estimation as a joint optimization problem integrating representation learning with Conditional Flow Matching (CFM). RepFlow mitigates selection bias by minimizing the entropically regularized Wasserstein distance between treated and control representations. To enhance numerical stability, we further introduce an $L_2$ normalization constraint on latent representations. This balanced representation enables the flow model to accurately capture the distribution of potential outcomes. Extensive experiments across a wide range of benchmarks demonstrate that RepFlow consistently outperforms existing methods in both point and distributional causal effect estimation.

Causal reasoning in natural language requires identifying relevant variables, understanding their interactions, and reasoning about effects and interventions, often under noisy or ambiguous conditions. While large language models (LLMs) exhibit strong general reasoning abilities, they struggle to disentangle correlation from causation, particularly when observations are partially incorrect or irrelevant information is present. In this work, we introduce NoisyCausal, a new benchmark designed to evaluate causal reasoning under structured noise. Each instance is generated from a ground-truth causal graph and contextualized with a natural language scenario by injecting controllable forms of noise, such as irrelevant distractors, value perturbations, confounding, and partial observability. Moreover, we propose a modular reasoning framework that combines LLMs with explicit causal structure to address these challenges. Our method prompts the LLM to extract variables, construct a causal graph from context, and then reformulates the reasoning task as a structured prompt grounded in this graph. Rather than relying on statistical patterns alone, the LLM is guided by symbolic structure, enabling more interpretable and robust inference. Experimental results show that our method significantly outperforms standard prompting and reasoning baselines on NoisyCausal. Furthermore, it generalizes well to external benchmarks such as Cladder without task-specific tuning. Our findings highlight the importance of combining causal abstractions with language-driven reasoning to achieve faithful and robust causal understanding in LLMs.

This work establishes a foundational framework for standardizing AI evaluation RCTs (sometimes called human uplift studies). Drawing on established experimental practices from disciplines with established RCT traditions, including software engineering, economics, clinical and health sciences, and psychology, we adopt the (Shadish et al., 2002) four-validity framework and extend it with a fifth principle on transparency, repeatability, and verification adapted from the Transparency and Openness Promotion (TOP) Guidelines (Center for Open Science, 2025). We operationalize all five principles into 33 guidelines adapted for AI evaluation RCT contexts, expressed as requirements with rationales, implementation instructions, and evidence bases. We position the principles and guidelines as serving three key roles for AI evaluation RCTs: a design tool for planning studies, an evaluation rubric for assessing existing work, and a blueprint for standard setting as the field converges on norms. Our framework extends prior work by centering evaluation on human performance rather than model output alone, formalizing causal inference through RCT methodology for AI contexts, integrating heterogeneity analysis and practical significance assessment, implementing a graded transparency and repeatability framework, and addressing AI-specific challenges including model versioning, human-AI interaction dynamics, contamination and spillover effects, and equitable impact assessment.

Empirical causal claims depend on many analyst decisions, from selecting covariates to choosing estimators. Existing robustness tools summarize how results vary across these choices, but, to the best of our knowledge, do not answer: \textbf{How many analyst decisions must change to reach a specification, which is a set of choices, whose confidence interval (CI) contains zero?} We introduce \emph{Minimum Specification Perturbation (MSP)}, the smallest number of changes. MSP is small under the null, grows with effect strength and captures distance-to-falsification information that dispersion-based summaries cannot report; when making decisions under weak effects, an MSP-based rule yields lower false-positive rates than dispersion-based rules. We show that Fragility Index and MSP measure orthogonal vulnerabilities: fragility to influential observations need not imply fragility to specification choices. On the LaLonde benchmark, MSP = 1 implies that one decision change makes the CI contain zero. We further provide exact permutation calibration under randomization and characterize computation, showing tractable cases under additive structure and NP-hardness in general.

The dominant noun-based modeling paradigm, grounded in probability theory and committed to pre-specified noun entities as primitive modeling units, is insufficient as a \emph{grammar of thought}: It leaves \emph{timing} outside the computational scope, precluding any adequate representation of the future as an open space of possibilities. This paper addresses three conceptual gaps absent from the existing literature: (1) possibility space -- a framework admitting multiple possible timelines for the same event; (2) timing computation -- the treatment of timing as a computable rather than observed dimension; and (3) causal factum -- the maximal causal efficacy recovered by reasoning backward from possible futures, rather than assumed in advance. Together, these definitions dissolve the confounding problem inherent to noun-based causal inference and provide the foundation for a spontaneously growing causal-reasoning world model. As proof of concept, we instantiate the framework and apply it to longitudinal EHR data from 3,276 breast cancer patients, demonstrating for the first time, to our knowledge, automatic trajectory discovery and counterfactual timing deduction (i.e., a What-If Machine) in a purely data-driven manner.

Causal inference is essential for data-driven decision-making, as it aims to uncover causal relationships from observational data. However, identifying causality remains challenging due to the potential for confounding and the distinction between correlation and causation. While recent advances in causal machine learning and matching algorithms have improved estimation accuracy, these methods often face trade-offs between interpretability and computational efficiency. This paper proposes a novel approach that combines a tree-based discretization technique, tailored for causal inference, with an integer linear programming-based matching algorithm. The discretization ensures approximately linear relationships for control datasets within strata, enabling effective matching, while the optimization framework optimizes for global balance. The resulting algorithm yields computational efficiency and less biased ATT estimates compared to state-of-the-art algorithms. Empirical evaluations demonstrate the proposed method's practical advantages over existing techniques in causal inference scenarios.

Detectors often suffer from degraded performance, primarily due to the distributional gap between the source and target domains. This issue is especially evident in single-source domains with limited data, as models tend to rely on confounders (e.g., illumination, co-occurrence, and style) from the source domain, leading to spurious correlations that hinder generalization. To this end, this paper proposes a novel Basis-driven framework for domain generalization, namely \textbf{\textit{Bridge}}, that incorporates causal inference into object detection. By learning the low-rank bases for front-door adjustment, \textbf{\textit{Bridge}} blocks confounders' effects to mitigate spurious correlations, while simultaneously refining representations by filtering redundant and task-irrelevant components. \textbf{\textit{Bridge}} can be seamlessly integrated with both discriminative (e.g., DINOv2/3, SAM) and generative (e.g., Stable Diffusion) Vision Foundation Models (VFMs). Extensive experiments across multiple domain generalization object detection datasets, i.e., Cross-Camera, Adverse Weather, Real-to-Artistic, Diverse Weather Datasets, and Diverse Weather DroneVehicle (our newly augmented real-world UAV-based benchmark), underscore the superiority of our proposed method over previous state-of-the-art approaches. The project page is available at: https://mingbohong.github.io/Bridge/.

Synthetic tabular data are often evaluated by distributional similarity, privacy distance, or train-on-synthetic-test-on-real predictive performance, but these criteria do not ensure validity for causal inference. We show that fully generative tabular synthesizers, including GAN- and LLM-based models, can preserve predictive utility while distorting average treatment effect (ATE) estimates. The failure is structural: ATE preservation requires both a realistic covariate law and an accurate treatment-effect contrast, whereas prediction loss penalizes treatment-effect error only through an overlap-weighted term. Thus, under imbalance or limited overlap, a generator may reproduce dominant observed outcomes while underlearning intervention-relevant contrasts. We formalize this mismatch through sensitivity and loss-decomposition results. Motivated by this causal analysis and intuition, we propose a hybrid synthetic-data framework for causal inference that generates covariates while modeling treatment and outcome mechanisms separately. We evaluate the framework in three settings: ATE preservation under fully generative versus hybrid synthesis, augmentation for practical positivity problems, and diagnostic simulation engines for comparing OR, IPW, AIPW, and TMLE before real-data analysis. We also stress-test the hybrid construction across settings that vary overlap, covariate dimension, seed sample size, and treatment-effect complexity, including a logistic outcome-model misspecification check. Across controlled simulation experiments, hybrid synthesis improves causal fidelity relative to fully generative baselines; the ACTG application shows improved predictive fidelity and potential for finite-sample estimator benchmarking. LLM-based hybrid synthesis is often more faithful than CTGAN in settings where causal fidelity can be assessed.

Causal effect estimation from observational data requires careful adjustment for confounding. Classical estimators such as inverse probability weighting and augmented inverse probability weighting are effective under favorable model specification, but may become unstable when treatment assignment and outcome mechanisms are complex, non-linear, and high-dimensional. Machine learning and representation learning approaches improve flexibility, yet joint training can allow outcome-related information to influence treatment-side representations, which is undesirable from a causal perspective. We propose MOCA (Modular One-way Causal Attention), a transformer-based framework that separates treatment and outcome modeling through a modular design, and performs confounder adjustment using a one-way attention mechanism. A cutting-feedback strategy, implemented via gradient detachment, prevents the outcome loss from updating the treatment module. This design preserves directional information flow while retaining the representational power of transformer architectures for causal inference. Across multiple simulated scenarios, including linear, nonlinear, heavy-tailed, hidden confounding, and high-dimensional settings, MOCA shows competitive or improved performance relative to IPW, AIPW, X-learner, TARNet, and DragonNet. We further illustrate the method on the Infant Health and Development Program dataset and the Dehejia-Wahba dataset as real-world benchmarks. These results suggest that modular attention with one-way information flow provides a promising and interpretable direction for causal inference with modern deep learning models.

Latent variables pose a fundamental challenge to causal discovery and inference. Conventional local methods focus on direct neighbors but fail to provide macro level insights. Cluster level methods enable macro causal reasoning but either assume clusters are known a priori or require causal sufficiency. Moreover, directly applying single variable causal discovery methods to cluster level problems violates causal sufficiency and leads to incorrect results. To overcome these limitations, this paper proposes L2C (Local to Cluster Causal Abstraction), a unified framework that bridges local structure learning and cluster level causal discovery. Unlike prior work that requires a complete manual assignment of micro variables to clusters, L2C discovers the partition automatically from local causal patterns. Our solution leverages a cluster reduction theorem to reduce any cluster to at most three nodes without loss of causal information, applies local causal discovery to identify direct causes, effects, and V structures in the presence of latent variables, and performs macro level causal inference via cluster level calculus on the learned cluster graph. L2C does not assume causal sufficiency, as latent variables are handled through local discovery. Theoretical analysis shows that L2C ensures soundness, atomic completeness, and computational efficiency. Extensive experiments on synthetic and real world data demonstrate that L2C accurately recovers ground truth clusters and achieves superior macro causal effect identification compared to existing baselines.

Determining identifiability of causal effects from observational data under latent confounding is a central challenge in causal inference. For linear structural causal models, identifiability of causal effects is decidable through symbolic computation. However, standard approaches based on Gröbner bases become computationally infeasible beyond small settings due to their doubly exponential complexity. In this work, we study how to practically use symbolic computation for deciding rational identifiability. In particular, we present an efficient algorithm that provably finds the lowest degree identifying formulas. For a causal effect of interest, if there exists an identification formula of a prespecified maximal degree, our algorithm returns such a formula in quasi-polynomial time.

Medical Visual Question Answering (MedVQA) aims to generate clinically reliable answers conditioned on complex medical images and questions. However, existing methods often overfit to superficial cross-modal correlations, neglecting the intrinsic biases embedded in multimodal medical data. Consequently, models become vulnerable to cross-modal confounding effects, severely hindering their ability to provide trustworthy diagnostic reasoning. To address this limitation, we propose a novel Dual Causal Inference (DCI) framework for MedVQA. To the best of our knowledge, DCI is the first unified architecture that integrates Backdoor Adjustment (BDA) and Instrumental Variable (IV) learning to jointly tackle both observable and unobserved confounders. Specifically, we formulate a Structural Causal Model (SCM) where observable cross-modal biases (e.g., frequent visual and textual co-occurrences) are mitigated via BDA, while unobserved confounders are compensated using an IV learned from a shared latent space. To guarantee the validity of the IV, we design mutual information constraints that maximize its dependence on the fused multimodal representations while minimizing its associations with the unobserved confounders and target answers. Through this dual mechanism, DCI extracts deconfounded representations that capture genuine causal relationships. Extensive experiments on four benchmark datasets, SLAKE, SLAKE-CP, VQA-RAD, and PathVQA, demonstrate that our method consistently outperforms existing approaches, particularly in out-of-distribution (OOD) generalization. Furthermore, qualitative analyses confirm that DCI significantly enhances the interpretability and robustness of cross-modal reasoning by explicitly disentangling true causal effects from spurious cross-modal shortcuts.

Multimodal affective computing aims to predict humans' sentiment, emotion, intention, and opinion using language, acoustic, and visual modalities. However, current models often learn spurious correlations that harm generalization under distribution shifts or noisy modalities. To address this, we propose a causal modality-invariant representation (CmIR) learning framework for robust multimodal learning. At its core, we introduce a theoretically grounded disentanglement method that separates each modality into causal invariant representation' and environment-specific spurious representation' from a causal inference perspective. CmIR ensures that the learned invariant representations retain stable predictive relationships with labels across different environments while preserving sufficient information from the raw inputs via invariance constraint, mutual information constraint, and reconstruction constraint. Experiments across multiple multimodal benchmarks demonstrate that CmIR achieves state-of-the-art performance. CmIR particularly excels on out-of-distribution data and noisy data, confirming its robustness and generalizability.

Causal inference from electronic health records (EHR) is fundamentally limited by unmeasured confounding: critical clinical states such as frailty, goals of care, and mental status are documented in free-text notes but absent from structured data. Large language models can extract these latent confounders as interpretable, structured covariates, yet how to effectively integrate them into causal estimation pipelines has not been systematically studied. Using the MIMIC-IV database with 21,859 sepsis patients, we compare seven covariate-integration strategies for estimating the effect of early vasopressor initiation on 28-day mortality, spanning tabular-only baselines, traditional NLP representations, and three LLM-augmented approaches. A central finding is that not all integration strategies are equally effective: directly augmenting the propensity score model with LLM covariates achieves the best performance, while dual-caliper matching on text-derived categorical distances restricts the donor pool and degrades estimation. In semi-synthetic experiments with known ground-truth effects, LLM-augmented propensity scores reduce estimation bias from 0.0143 to 0.0003 relative to tabular-only methods, and this advantage persists under substantial simulated extraction error. On real data, incorporating LLM-extracted covariates reduces the estimated treatment effect from 0.055 to 0.027, directionally consistent with the CLOVERS randomized trial, and a doubly robust estimator yielding 0.019 confirms the robustness of this finding. Our results offer practical guidance on when and how text-derived covariates improve causal estimation in critical care.

Large language models enable inexpensive AI-generated annotations, but using them reliably for causal inference remains challenging. Naively pooling AI and human data induces bias, while existing methods such as Prediction-Powered Inference (PPI; Angelopoulos et al., 2023a) treat AI outputs as proxies of true labels -- an assumption often violated for generative model outputs in practice. We propose Generative Augmented Inference (GAI), a framework that treats AI outputs as general, potentially high-dimensional informative features for learning human labels rather than as surrogates. GAI flexibly models this relationship using nonparametric methods, enabling consistent estimation and valid inference from combined human and AI data. We establish asymptotic normality and show that, under random labeling, GAI strictly improves asymptotic efficiency over human-data-only estimation whenever AI outputs are informative for true labels. Empirical studies on real-world datasets demonstrate that GAI significantly reduces estimation error and improves confidence interval quality across diverse generative data sources relative to human-only and PPI-based estimation.

Young children demonstrate early abilities to understand their physical world, estimating depth, motion, object coherence, interactions, and many other aspects of physical scene understanding. Children are both data-efficient and flexible cognitive systems, creating competence despite extremely limited training data, while generalizing to myriad untrained tasks -- a major challenge even for today's best AI systems. Here we introduce a novel computational hypothesis for these abilities, the Zero-shot World Model (ZWM). ZWM is based on three principles: a sparse temporally-factored predictor that decouples appearance from dynamics; zero-shot estimation through approximate causal inference; and composition of inferences to build more complex abilities. We show that ZWM can be learned from the first-person experience of a single child, rapidly generating competence across multiple physical understanding benchmarks. It also shows progressive, staged emergence of capacities during learning and builds brain-like internal representations. Our work presents a blueprint for efficient and flexible learning from human-scale data, advancing both a computational account of children's early physical understanding and a path toward data-efficient AI systems.

Selective conformal prediction can yield substantially tighter uncertainty sets when we can identify calibration examples that are exchangeable with the test example. In interventional settings, such as perturbation experiments in genomics, exchangeability often holds only within subsets of interventions that leave a target variable "unaffected" (e.g., non-descendants of an intervened node in a causal graph). We study the practical regime where this invariance structure is unknown and must be estimated from data. Our main result quantifies how coverage degrades when the estimated safe calibration set accidentally includes interventions that affect the target, and gives a conservative correction when an upper bound on this error is available. Rather than learning a full causal graph, we learn only the intervention-target relationships needed to choose calibration interventions. We give algorithms for this partial learning task and evaluate them on synthetic structural equation models and Replogle K562 CRISPR-interference data, where the experiments illustrate synthetic gains from selective calibration and finite-sample tradeoffs on real perturbation screens.

A fundamental challenge in causal inference with observational data is correct specification of a causal model. When there is model uncertainty, analysts may seek to use estimates from multiple candidate models that rely on distinct, and possibly partially overlapping, sets of identifying assumptions to infer the causal effect, a process known as triangulation. Principled methods for triangulation, however, remain underdeveloped. Here, we develop a framework for causal effect triangulation that combines model testability methods from causal discovery with statistical inference methods from semiparametric theory, while avoiding explicit model selection and post-selection inference problems. We propose a triangulation functional that combines identified functionals from each model with data-driven measures of model validity. We provide a bound on the distance of the functional from the true causal effect along with conditions under which this distance can be taken to zero. Finally, we derive valid statistical inference for this functional. Our framework formalizes robustness under causal pluralism without requiring agreement across models or commitment to a single specification. We demonstrate its performance through simulations and an empirical application.

Empirical investigations into unintended model behavior often show that the algorithm is predicting another outcome than what was intended. These exposés highlight the need to identify when algorithms predict unintended quantities - ideally before deploying them into consequential settings. We propose a falsification framework that provides a principled statistical test for discriminant validity: the requirement that an algorithm predict intended outcomes better than impermissible ones. Drawing on falsification practices from causal inference, econometrics, and psychometrics, our framework compares calibrated prediction losses across outcomes to assess whether the algorithm exhibits discriminant validity with respect to a specified impermissible proxy. In settings where the target outcome is difficult to observe, multiple permissible proxy outcomes may be available; our framework accommodates both this setting and the case with a single permissible proxy. Throughout we use nonparametric hypothesis testing methods that make minimal assumptions on the data-generating process. We illustrate the method in an admissions setting, where the framework establishes discriminant validity with respect to gender but fails to establish discriminant validity with respect to race. This demonstrates how falsification can serve as an early validity check. We also provide analysis in a criminal justice setting, where we highlight the limitations of our framework and emphasize the need for complementary approaches to assess other aspects of construct validity and external validity.

Causal inference in spatial domains faces two intertwined challenges: (1) unmeasured spatial factors, such as weather, air pollution, or mobility, that confound treatment and outcome, and (2) interference from nearby treatments that violate standard no-interference assumptions. While existing methods typically address one by assuming away the other, we show they are deeply connected: interference reveals structure in the latent confounder. Leveraging this insight, we propose the Spatial Deconfounder, a two-stage method that reconstructs a substitute confounder from local treatment vectors using a conditional variational autoencoder (C-VAE) with a spatial prior, then estimates causal effects with a flexible outcome model. We show that this enables nonparametric identification of direct and spillover effects under weak assumptions--without multiple treatment types or a known latent-field model. Empirically, we extend SpaCE, a benchmark suite for spatial confounding, to include treatment interference, and show that the Spatial Deconfounder consistently improves effect estimation across real-world environmental health and social science datasets. By turning local interference into a multi-cause proxy for latent spatial confounding, our framework advances robust causal inference for spatial data.

Fair machine learning seeks to identify and mitigate biases in predictions against unfavorable populations characterized by demographic attributes, such as race and gender. Recent research has extended fairness to graph data, such as social networks, but many studies neglect the causal relationships among data instances. This paper addresses a prevalent challenge in many fair machine learning research, which typically assumes independent and identically distributed (IID) data, from the causal perspective. Specifically, this work targets the circumstance where nodes with different neighborhood structures follow different causal mechanisms, violating the invariance assumptions required for classical structural causal models and do-calculus. We base our research on the Network Structural Causal Model (NSCM) framework and develop a Message Passing Variational Autoencoder for Causal Inference (MPVA) to compute interventional distributions for causally fair node classification. We establish theoretical soundness under two conditions: Decomposability and Graph Independence. These conditions formalize when causal mechanism heterogeneity can be overcome by constructing a structural representation that restores invariance and facilitates the computation of interventional distributions using do-calculus in non-IID settings. Empirical evaluations on semi-synthetic and real-world datasets demonstrate that MPVA outperforms conventional methods by effectively approximating interventional distributions and mitigating bias. Our findings demonstrate the potential of causality-based fairness in complex ML applications and motivate future work on relaxing the classic assumptions in algorithmic fairness.