Causal Inference
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21 papers in the last four weeks, up 62% on the four weeks before. 0.2% of all new papers.
Latest papers 222
From climate teleconnections to gene regulation, modern time-series datasets encompass tens or hundreds of interacting variables, making causal discovery increasingly challenging. Constraint-based methods offer statistical rigor but their nonlinear CI tests are infeasible at scale, while score-based alternatives avoid CI testing but require arbitrary thresholds to binarize continuous edge scores. We propose GRACE (ated efinement for ccurate ausal dge discovery), which refines constraint-based discovery using Hard Concrete gates with regularization: each candidate edge has an independent gate whose values concentrate near 0 or 1, yielding a clean bimodal separation that makes the binary decision robust, unlike the narrow, overlapping score distributions produced by and attention-based methods. A fast linear CI skeleton provides high-recall candidates; a single gated model then prunes false positives by learning which edges genuinely improve prediction, with automatic regularization adapted to problem dimensions and skeleton density. Systematic experiments on synthetic benchmarks, spanning diverse graph topologies (scale-free, Erdős-R'enyi, small-world) and dimensionalities up to , show that GRACE substantially improves F1 over its base CI method while maintaining high precision, and outperforms attention-based and score-based alternatives. GRACE matches or exceeds expensive nonlinear CI tests at a fraction of the cost ( faster). On a real-world river flow dataset, where rainfall confounders, variable propagation lags, and distributional shifts violate standard assumptions, a temporal bootstrap variant of GRACE recovers 9 of 11 causal edges along the Elbe River with only 1 false positive (, AUROC), reducing the skeleton's 106 false positives by 99%.
One Ruler: A Same-Hands Re-Evaluation of Bivariate Causal Direction on Tuebingen, with a Parameter-Free Compression Baseline
Headline accuracies on the Tuebingen cause-effect pairs are routinely compared across papers even though each is measured under its authors' own protocol -- different pair subsets, weightings, model-selection, and decision rates. We argue this is the wrong comparison and run the right one: a same-hands re-evaluation in which every method is run by us on the identical 102 pairs, with one strict rule -- no tuning and a decision forced on every pair. As a clean reference point we introduce a deliberately minimal baseline: sorted-conditional compression, which feeds quantized, sorted, first-differenced data to an off-the-shelf compressor (bz2) and has zero fitted parameters. Under the common ruler the ranking differs sharply from the literature. Our baseline reaches 74.7% weighted accuracy (p = 3.7e-7); on the same 100 pairs that SLOPE is evaluated on it scores 76.0%, a 1.2-point gap below the authors' own forced-decision SLOPE (77.2%) that is well inside noise (McNemar p = 0.39). A faithful re-run of RECI lands at 70.7% -- inside the original authors' reported error bar, not the 77.5% often quoted (which we trace to a mis-copied cell). SLOPE's published 82.4% is a decided-subset figure: scoring the authors' own stored output only on the pairs its significance test chose to answer reproduces 81.7%. Under the common ruler the methods cluster in the low-to-mid 70s and the zero-parameter compressor ties the strongest of them. We document the mechanisms that inflate published figures (test-set model selection, significance-gated abstention) and contribute two further results: compression score magnitude is a model-free confounding flag (p = 2.8e-68), and a pre-registered falsification test fails in an instructive way that bounds the method's theoretical interpretation. Code, pre-registrations, and per-pair outputs are released.
Statistical Inference for Misspecified Contextual Bandits
Contextual bandit algorithms have transformed modern experimentation by enabling real-time adaptation for personalized treatment. Yet these advantages create challenges for statistical inference due to adaptivity. We study inference with contextual-bandit data without assuming a well-specified outcome model. In this setting, we show a previously overlooked issue: standard algorithms such as LinUCB may fail to stabilize under misspecified working models, leading to non-Gaussian estimator behavior and invalid inference. This issue is practically important, as misspecified working models -- such as approximations of complex dynamical systems -- are often employed by online agents in real-world adaptive experiments to balance reward, computational tractability, and robustness. We develop an inverse-probability-weighted Z-estimation framework for a broad class of marginal moment targets, including projection parameters, structural parameters with noisy contexts, and off-policy values. We identify a stability condition tailored to this framework, scaled inverse-propensity convergence, under which the IPW-Z estimator is consistent and asymptotically normal with a consistent sandwich variance estimator. We further establish sufficient conditions for scaled inverse-propensity convergence for several policy classes, including multi-armed bandit algorithms and smooth contextual allocation policies. Simulations and a HeartSteps V1 real-data-calibrated application show reliable coverage and competitive performance across multiple targets. Overall, our results highlight the importance of stability-aware adaptive design for valid post-experiment inference.
A Survey on Federated Causal Discovery and Inference
Causal reasoning, which encompasses the discovery of causal structures and the inference of causal effects, is fundamental to data-driven decision making. In practice, data for reliable causal analysis are often distributed across institutions and cannot be centralized due to privacy regulations or communication constraints. Federated learning (FL) addresses this by enabling collaborative analysis without raw data sharing, giving rise to the rapidly growing field of federated causal discovery (FCD) and inference (FCI). However, the interdisciplinary nature of this field and the absence of a comprehensive survey present barriers to entry for researchers. This paper bridges that gap by providing a systematic review through multi-dimensional taxonomies. Grounded in the three core design decisions underlying any FCD solution, namely how structures are learned, how data are partitioned, and what structural knowledge each party obtains, we organize FCD along three axes: methodological paradigm, federation topology, and structural scope. We further examine key practical dimensions, including temporal dynamics, data heterogeneity, missing data, and non-identical variable sets. For FCI, we categorize methods by target estimand (average versus individualized/conditional treatment effects) and by estimation strategy, from classical weighting methods to modern deep generative architectures. Unlike prior works that treat FCD and FCI separately, we formalize their connection as complementary stages of a unified federated causal reasoning pipeline, where FCD supplies the structural knowledge required for valid effect estimation in FCI. Finally, we highlight their shared concerns regarding privacy, communication efficiency, theoretical guarantees, and application domains, and conclude by identifying open challenges for future research.
Fed-CausalDiff: Decoupled Synchronization for Federated Do-Simulation and Policy Evaluation
While federated learning enables collaborative modelling on decentralised data, standard methods merely fit historical observations. This purely observational approach is fundamentally insufficient for interventional inference and policy evaluation, as sequential actions dynamically alter future states. We propose \textbf{Fed-CausalDiff}, a federated causal diffusion framework for do-simulation. The architecture decomposes the evolution of the latent state into a global causal score function and a local confounding score function. This design enables \emph{decoupled synchronisation} (DSS), where clients aggregate only the shared causal mechanism while retaining site-specific confounders locally to handle heterogeneity. Experiments on four datasets demonstrate that Fed-CausalDiff achieves better ATE and policy-value estimation accuracy, offering a favorable trade-off between communication cost and inference fidelity.
Causal Gaussian Processes for Robust Treatment Effect Evaluation with Unobserved Confounding
The presence of confounding bias poses a key challenge in policy evaluation, as the target causal effects of actions are not identifiable (i.e., underdetermined) from observational data. On the other hand, existing confounding-robust evaluation strategies require detailed prior knowledge about the environment or apply only to discrete treatments and outcomes. This paper investigates causal effect evaluation over the continuous domain from confounded observations, while requiring only basic temporal ordering between the treatment and the outcome. We introduce a universal discretization of the exogenous domains that approximates the observational and interventional distributions of any causal model with arbitrary accuracy using a finite number of latent states. Building on this newfound universal approximation property, we develop a novel family of Causal Gaussian process (CGP) models that effectively approximate the observational and interventional distributions of any causal model with confounded observations.
Causal Variational Deep Embedding: A Family of Interventional Generators for Confounded Images
Deep generative models reproduce the observational distribution of their training data, inheriting any spurious associations it contains. A common source is an unobserved confounder that shapes both an attribute the user wants to control at sampling time and an attribute expected to vary in response. Existing causal generative approaches resolve the resulting ambiguity by imposing structural assumptions strong enough to single out one interventional distribution; in image domains, such assumptions are rarely warranted, and the data is generally consistent with a set of distinct causal mechanisms -- a feasible region of interventional distributions. We propose CauVaDE (Causal Variational Deep Embedding), built on a canonical augmented SCM in which the unobserved confounder collapses, without loss of generality, into a discrete latent cluster of bounded support while continuous variation is absorbed into independent noises. We prove that this canonical class is dense, in both observational and interventional Wasserstein distance, in the class of augmented SCMs compatible with a given causal diagram, and instantiate it as a mixture variational autoencoder whose cluster variable plays the role of the canonical confounder. An entropy regularizer with weight on the cluster posterior then traces a family of candidate causal effects that fit the observational data to comparable likelihood while spanning the feasible region. Experiments on image data benchmarks show that CauVaDE produces diverse interventional samples and improves FID against an unconfounded reference.
Root Cause Analysis with Latent Confounders using Partial Ancestral Graphs
Finding the source of failures, known as Root Cause Analysis (RCA), is essential for identifying the root causes of anomalies and maintaining the reliability of complex systems. While causal theory has advanced data-driven RCA, existing frameworks assume causal sufficiency, failing to account for the unobserved latent variables prevalent in real-world environments. To address this gap, we propose PAG-RCA. This framework models system failures as parametric interventions over Partial Ancestral Graphs (PAGs) to perform RCA in the presence of latent variables. We use standard causal identification algorithms to find the source of failures by quantifying causal effects over the PAG. When an effect is identifiable, candidate root causes are ranked based on their exact intervention effects. When effects are structurally unidentifiable, our framework (for the first time in the RCA literature) integrates partial identification to evaluate and score candidates using analytical causal bounds. By integrating latent variables and partial identification at once our framework ensures robust RCA even under data scarcity and latent-variable scenarios where traditional methods degrade. Evaluations on synthetic data, microservice anomaly benchmarks and power-grid cascading failures demonstrate that PAG-RCA consistently outperforms state-of-the-art data-driven baselines. By improving data-driven RCA performance under data scarcity, this methodology advances reliable automated diagnostics in partially observable complex networks.
Wasserstein Policy Learning for Distributional Outcomes
Offline policy learning has received growing attention in causal inference. The primary objective is to learn a policy (individualized treatment rule) as a mapping from covariates to treatment that maximizes the empirical welfare defined as the mean of scalar-valued potential outcomes. In this paper, we study offline policy learning with distribution-valued outcomes, where each potential outcome is a probability measure on and the reward is defined through a utility functional applied to the Wasserstein barycenter of induced outcome distributions. We establish statistical guarantees for the policy learning framework based on both Inverse Probability Weighting (IPW) and Doubly Robust (DR) estimators. By handling the challenging uniform deviation over the product of the combinatorial policy class and the infinite-dimensional quantile domain, we prove that the finite-sample regret has leading dependence . In the one-dimensional Wasserstein setting and under the stated regularity conditions, the leading regret rate is still governed by the policy-class complexity. Moreover, we provide a minimax lower bound establishing the sharpness of the leading dependence on and .
Identifying Structural Biases from Causal Mechanism Shifts
Causal discovery methods commonly assume that all data is independently and identically distributed (i.i.d.) and that there are no unmeasured variables affecting the system. In practice, these assumptions are often violated, leading to inaccurate inference. In this paper, we study how to identify hidden confounding and selection biases from causal mechanism shifts. In particular, we show that structural biases lead to dependent mechanism shifts. That is, by considering for which variables the mechanisms change given data from different environments, we can tell which variables are unbiased, which are subject to hidden confounding, and which are undergoing selection bias. We formalize this into an empirically testable criterion based on mutual information, and show under which conditions it identifies structural biases. To tell which nodes are subject to what kind of bias, we introduce the StruBI algorithm. Experiments on synthetic and real-world data show that StruBI works well in practice, accurately recovering affected variable sets and types of biases, outperforming the state-of-the-art by a wide margin.
Shrinkage priors for Bayesian Substitute Confounders
Multi-cause observational studies contain information about unmeasured confounding through the dependence structure among causes. However, literal imputation of the unobserved confounder is often more complex than learning a lower-dimensional substitute score that preserves the shared assignment variation needed for stable causal adjustment. The deconfounder (Wang and Blei, 2019) and related substitute confounder methods exploit this idea, but flexible assignment models can fit the joint distribution of the causes while producing scores that over-encode the treatment vector, collapse overlap, or capture single-cause variation. We develop a Bayesian factor assignment framework for learning sparse substitute confounders that retain coarse multi-cause dependence with shrinkage priors. The theory is stated at the level of posterior concentration, factor score contraction, and overlap-preserving assignment geometry and therefore does not rely on a particular shrinkage prior. Under these conditions, the proposed regression-adjusted estimators are consistent for mean potential outcomes when the corresponding latent variable identification assumptions hold. Shrinkage priors provide a natural tool for latent structural learning: they favour low-dimensional factors supported by multiple causes, discourage effectively single-cause factors, and induce an ordering of the latent factors through progressive shrinkage. Synthetic experiments illustrate the roles of signal strength, outcome validity, and geometry-aware regularization. In an Alzheimer's Disease Neuroimaging Initiative (ADNI) baseline analysis, sparse substitute scores recover much of the adjustment obtained by directly conditioning on invasive cerebrospinal-fluid biomarkers, while collapse diagnostics identify when fitted factors reduce to individual observed measurements.
Fast Nonparametric Conditional Independence Testing via Two-Stage Regression
Constraint-based causal discovery relies on repeated conditional independence tests, but fast nonparametric tests often sacrifice calibration, especially when variables depend on the conditioning set through nonlinear relationships. We introduce BLITZ (Broad-to-Local Independence Testing via residualiZation), a nonparametric conditional independence test designed to run well under a second while maintaining the accuracy needed for the thousands of queries performed by constraint-based causal discovery algorithms. BLITZ first removes broad smooth dependence on the conditioning set using low-order polynomial regression, then applies a small nonlinear feature map and residualizes those features with shallow tree regressions. The resulting statistic tests residual cross-covariance, with a moment-matched chi-square approximation to the null distribution. We show theoretically that the two-stage design reduces the effective complexity faced by the tree residualizers, allowing shallow trees to control residual conditional-mean bias while avoiding excessive overfitting. In simulations, BLITZ provides better null calibration than fast kernel, random-feature, and regression-based competitors while remaining among the fastest methods tested. In causal discovery experiments on synthetic graphs and flow-cytometry data, BLITZ yields more reliable endpoint orientations among retained adjacencies and competitive structural recovery. These results suggest that broad-to-local residualization is a practical route to calibrated, scalable nonparametric conditional independence testing for causal discovery.
Statistical Foundations of LLM-based A/B Testing: A Surrogacy Framework for Human Causal Inference
Organizations and researchers show increasing interest in using large language models (LLMs) in place of human participants in A/B tests, in the hope of experimenting faster and at lower cost. We study when a treatment effect estimated on LLM outcomes can recover the effect for the human population of interest. Distributional equivalence between LLM and human outcomes would make any standard estimator valid but is unrealistic. We therefore develop a statistical framework that adapts surrogate endpoint theory to LLMs, showing that calibrating LLM outcomes to human outcomes identifies the average treatment effect under surrogacy and comparability conditions that are jointly weaker than distributional equivalence. We present a falsification test for surrogacy and a bound on the worst-case bias from limited overlap between the LLM and human samples. We further show that the stochasticity inherent to LLMs can weaken surrogacy for identification while also introducing bias and variance during estimation, but that using an average over multiple LLM draws per unit as the surrogate mitigates these issues. Simulations validate the results, and an empirical application to the Upworthy Research Archive dataset shows that raw LLM outputs recover only 39% of the human treatment effect while nonparametric calibration closes the gap. A central takeaway is that A/B testing on LLM responses is correct only by assumption, whereas A/B testing on humans is correct by design, and that the required assumptions are hardest to justify precisely where LLMs promise the greatest benefit. We discuss the choice of LLM, prompting, and temperature as design variables, the compounded challenge posed by long-term outcomes, and how to size human pilot studies for validation.
The Critical Role of Model Selection in Causal Inference: A Comparative Analysis of Classification Models within the InferBERT Framework for Pharmacovigilance
Distinguishing causal adverse drug events (ADEs) from spurious correlations remains a central challenge in pharmacovigilance. The InferBERT framework integrates transformer models with Do-calculus, but its success hinges on the underlying classification model. This study evaluates the impact of model choice in InferBERT, assessing whether simpler models suffice, if domain-specific pre-training helps, whether scaling to LLMs improves causal detection, and the effect of post-hoc calibration. We performed a comparative study on two benchmarks: Analgesics-induced Acute Liver Failure (AILF) and Tramadol-related Mortalities (TRAM). Four models were evaluated-XGBoost (baseline), ALBERT (original InferBERT), BioBERT (biomedical transformer), and Med-LLaMA (medical LLM)-using 5-fold cross-validation repeated over 20 runs. We measured accuracy, Expected Calibration Error (ECE) pre- and post-isotonic regression, and Jaccard concordance of causal terms with PRR, ROR, and EBGM; significance was tested with paired t-tests. BioBERT achieved the highest accuracy on both datasets, while Med-LLaMA underperformed despite its size and parameter-efficient fine-tuning. Domain-specific pre-training was decisive. Calibration improved ECE but had mixed effects on accuracy and causal discovery. BioBERT's superiority also yielded the strongest concordance with traditional pharmacovigilance signals. These results show that domain-specific pre-training provides a clear advantage over simpler baselines and larger LLMs. Investing in manageable, domain-aware models is more effective for computational pharmacovigilance than simply scaling model size.
Relational Structural Causal Models
An artificial intelligence must have a model of its environment that is causal, supporting reasoning about interventions and counterfactuals, and also combinatorial, supporting generalization to unseen combinations of objects. In this work, we formally study when and how such a model can be learned. We develop relational structural causal models, extending structural causal models (Pearl 2009) to settings where objects and their relations vary. First, we show how answers to not only causal but also observational queries about unseen combinations of objects can not be identified without further assumptions. To enable such identification--including in the presence of unobserved confounding--we define relational causal graphs and derive symbolic identification criteria. Finally, we propose relational neural causal models, a provably correct approach that outperforms non-relational baselines on simulated traffic scenes with varying cars, signals, and pedestrians.
Graph Diffusion Residuals for Control-Function Instrumental Variables
Control-function instrumental variable estimators need a first-stage residual, not merely a first-stage prediction. High-capacity first stages can interpolate treatment and leave too little residual information for the outcome equation. We study Adaptive Anisotropic Instrumental Heat Flow (A-IHF), a deterministic graph-diffusion residual extractor for flexible control functions. A-IHF treats treatment as a signal on a graph of first-stage features, uses pilot diffusion to detect large treatment jumps, attenuates conductance across those jumps, and computes the generated control with a sparse graph resolvent. Its observational selection rule uses only , combining graph generalized cross-validation, roughness, residualized-treatment relevance, and graph-admissibility filtering. The analysis decomposes error into structural leakage, residual attenuation, and residualized treatment variation, yielding finite-sample bounds, graph-admissibility rates under latent piecewise-smooth geometry, and finite-path selection calibration. Across 54 synthetic benchmark cells with tuned graph, kernel, tree, boosting, series, and neural control-function baselines, guarded observational A-IHF has the lowest average structural-response MSE; the A-IHF family beats the best non-A-IHF baseline in 32 cells. Performance is strongest when the graph captures piecewise-smooth first-stage structure.
Capability Minimization as a Safety Primitive: Risk-Aware Causal Gating for Least-Privilege LLM Agents
Modern decision systems increasingly rely on learned components whose outputs may be confident yet wrong, exposing downstream actions to costly errors. We introduce Risk-Aware Causal Gating (RACG), a framework that decides whether to act on, defer, or abstain from a model's prediction by combining causal effect estimation with calibrated risk control. RACG models the causal pathway from candidate actions to outcomes and gates each decision according to an estimated counterfactual risk rather than raw predictive confidence. To make gating reliable, we derive distribution-free bounds on the probability of acting under high-risk conditions and show how these bounds translate into operating thresholds that satisfy user-specified safety constraints. We further propose an adaptive gating policy that adjusts to distribution shift by monitoring discrepancies between predicted and realized outcomes, tightening the gate when causal assumptions appear violated. Across simulated interventions and real-world decision benchmarks, RACG reduces high-cost errors substantially while preserving most of the utility of an ungated policy, and it outperforms confidence-based and selective-prediction baselines at matched abstention rates. Our results indicate that explicitly separating causal risk from predictive uncertainty yields decision systems that are both safer and more transparent, offering a principled mechanism for trustworthy automation in high-stakes settings.
Is It You or Your Environment? A Bayesian Inference Framework for Genomically-Anchored Personalized Physiological Interpretation
Personalized health AI systems face a fundamental cold-start problem: machine learning models for physiological interpretation require weeks of individual behavioral data before they can distinguish constitutional variation from environmentally driven deviation. We propose a solution grounded in causal inference and Bayesian prior design. An individual's genomic profile serves as an exogenous genetic anchor -- a domain-informed, personalized prior that is fixed at conception, immune to reverse causation, and available before a single behavioral observation is collected. The anchor initializes a Bayesian belief state over an individual's physiological set point G-hat = mu + sum(beta_i * g_i), where beta_i are GWAS-derived effect sizes and g_i are risk-allele counts. Each incoming physiological measurement P produces a non-constitutional deviation delta = P - G-hat that separates the signal attributable to environment and state from the constitutionally fixed baseline. As behavioral data accrue, the prior decays according to G-hat_t = w(t)*G-hat_genomic + [1-w(t)]*P-bar_t, transitioning from genome-dominated to empirical-baseline-dominated inference. The same observed HRV of 55 ms generates a suppression hypothesis for a person whose prior predicts 80 ms, and an enhancement hypothesis for a person whose prior predicts 30 ms -- a reversal impossible without a personalized anchor. We develop this architecture across six physiological domains, grading genomic priors by evidence strength, distinguishing robustly replicated anchors (FTO, FADS1/2, FKBP5) from contested candidate genes (SLC6A4, MAOA, DRD2). We address the inference boundary between association, Mendelian randomization, and individual token causation, and define four constraints for deployment: evidence-graded priors, dynamic decay, ancestry-matched effect sizes, and attribution rather than deterministic output.
NetCause: Counterfactual Learning for Root Cause Analysis in Large-Scale Networks
Can a learned model capture how faults propagate through a large-scale network and use this knowledge to causally attribute customer impact to its underlying root cause? Existing root cause analysis techniques often rely on static rules, correlation heuristics, or topology-local reasoning, which struggle to generalize in dynamic environments where faults propagate across complex physical and logical dependencies. We present NetCause, a self-supervised learning-based framework that models network incidents as graph-temporal processes and uses counterfactual simulation to rank candidate root causes. This approach produces an interpretable ranking of root cause hypotheses and integrates naturally with operator-defined mitigation and remediation actions. We train the model on over 1,500 incidents collected over six months from a leading cloud provider's production network and evaluate it on 31 expert-labeled incidents. NetCause consistently improves root cause ranking quality in the regime most relevant to operational decision-making, achieving a 16.1% accuracy improvement over a rule-based heuristic baseline. While training is computationally intensive, inference is lightweight, requiring only seconds of GPU runtime per incident (well below typical telemetry collection latencies).
Prediction-Powered Causal Inference by Automatic Debiased Machine Learning and Semi-Supervised Riesz Regression
This study investigates semiparametric efficient estimation of causal and structural parameters in a semi-supervised setting. In our setting, unlabeled auxiliary regressors are available in addition to labeled observations consisting of outcomes and regressors. Our goal is to construct estimators of causal and structural parameters whose asymptotic variances are smaller than those of estimators constructed using only labeled data. We refer to this framework as prediction-powered causal inference (PPCI). We first derive the efficient influence function and the efficiency bound, which imply that the use of auxiliary regressors can attain a smaller asymptotic variance than the efficiency bound attainable from labeled observations alone. Then, by combining the efficient influence function with the debiased machine learning (DML) framework, we propose methods that we call DML-PPCI. If we construct an estimating-equation estimator, we refer to the method as EE-DML-PPCI; if we construct a targeted-learning estimator, we refer to the method as TMLE-DML-PPCI. The asymptotic variances of both estimators match our derived efficiency bound. In the construction of the estimators, estimation of the efficient influence function plays an important role. In our study, the efficient influence function is also a Neyman orthogonal score, which depends on the Riesz representer and the regression function. For Riesz representer estimation, we develop semi-supervised generalized Riesz regression with convergence rate guarantees.
Artemis: Anatomy-Resolved inTervention for Eliminating Multimodal NeuroImage confounderS
Multimodal neuroimaging, integrating functional connectivity from fMRI and structural connectivity from DTI, enables non-invasive analysis of brain networks using graph neural networks. However, demographic factors such as age and sex systematically confound the relationship between brain connectivity and clinical outcomes, causing GNNs to exploit spurious shortcuts rather than learning causally invariant representations. While recent causal GNN methods introduce causality at the graph-modeling level, their causal mechanisms remain domain-agnostic without accounting for the real-world confounders inherent in clinical neuroimaging data. Moreover, brain networks are constructed from atlas-based parcellations where each region exhibits distinct sensitivity to demographic factors, necessitating region-aware adjustment. We propose Artemis, a region-level causal framework that bridges this gap with causal intervention at each brain region independently by learning region-specific confounder representations with lightweight parameters. Our adjustment comprehensively utilized the multimodal functional and structural features for graph reasoning as a plug-in module compatible with arbitrary GNN backbones. Experiments on three benchmarks, ADNI for disease diagnosis, OASIS for dementia staging, and HCP for sex classification, demonstrate consistent improvements over representative GNN-based baselines. Multiple supporting experiments further demonstrate statistical significance and neuroscientific interpretability.
WorldKernel: A World Model is the Coupling Kernel of Admissible Possible Worlds
A common assumption holds that enough observational and interventional data, given to a strong enough predictor, suffices. We report a failure mode that contradicts it. Across hundreds of structural causal models, on identified quantities a strong predictor and a Bayesian baseline both succeed, but on unidentified quantities (the couplings between counterfactual worlds) the predictor collapses to a point, on 28% of models to one no valid model can produce, while the truth is an admissible interval more data never narrows. The gap is structural: prediction cannot represent uncertainty over counterfactual couplings. We cast a world model as a single positive semidefinite coupling kernel K(T,T') over admissible worlds, whose diagonal is the ordinary posterior (what a predictor recovers) and whose off-diagonal is the cross-world coupling it cannot, which every counterfactual reads. The paper is the theory of that off-diagonal. It is real: two states with identical posteriors differ on a cross-world query, and the off-diagonal is the coupling that fixes counterfactuals. It can be bounded: positive semidefiniteness is partial-identifying information the marginals lack, and enforcing it bounds counterfactuals in polynomial time where the exact response-type program is intractable. Logical structure sharpens it: ontology axioms tighten the bound by up to a third, propagating to couplings they never touch. It can be acquired: targeted scars, constraints learned from encountered infeasibilities, close the gap several times faster than untargeted ones. Its full reconstruction is approximate counting of the admissible worlds, tractable below the Sly-Sun threshold and inapproximable above; we do not claim to beat the worst case.
Computational Identifiability
Identification conditions describe the computability of a target query or parameter of interest as a function of the type and amount of information available. In causal identification, this information is often expressed in the form of a causal graph, and data are observed or collected for some subset of variables in the graph. Target queries may be for a single effect alone or for a class of effects in a given model. The derivation of an identification algorithm then defines mathematically the process by which the desired causal effect(s) can be uniquely determined, theoretically, in expectation. Identifiability in expectation, or 'theoretical identifiability,' generally assumes asymptotic properties, infinite data, or other mathematically idealized conditions. In this paper, we explore a fundamental distinction between this theoretical, idealized notion of identifiability and a proposed alternative that is computation-bound. The framework we propose - 'computational identifiability' - is to instead define a finite computational search procedure for an empirical estimator. If this process finds an estimator empirically, within a desired error tolerance, then identifiability is satisfied, conditional on the specified assumptions of the search (i.e., a prior distribution over the parameters) and conditional on the search procedure itself. Through several experiments, we demonstrate how this framework allows us to answer fine-grained, practical identification questions, such as identification with small finite samples, with ambiguous graphical criteria, with mixed observational-interventional data, and across counterfactual data and estimands. Code is available at https://github.com/lbynum/metadentify.
MEC-Cox: Machine-Learning-Assisted Generalized Entropy Calibration for ATT Marginal Hazard-Ratio Estimation
Externally controlled survival trials are increasingly used when concurrent randomized controls are infeasible, particularly in oncology and rare-disease settings with time-to-event endpoints. We target an average-treatment-effect-on-the-treated (ATT)-type marginal hazard-ratio estimand, comparing treatment with counterfactual control in the treated trial population, and estimate it using inverse-probability-weighted (IPW) Cox regression. Valid inference is challenging because IPW Cox regression depends on the weights through both event contributions and risk-set averages, making flexible machine-learning nuisance estimation difficult to incorporate directly. Building on machine-learning-assisted generalized entropy calibration (MEC) by Lee and Kim (2026), we propose MEC-Cox for ATT-weighted IPW Cox regression. The method begins with normalized source-propensity-score odds weights for external controls and then applies Bregman calibration to balance cross-fitted prognostic summaries between external controls and treated trial patients. The calibration basis may include control-survival predictions, Cox linear predictors, penalized-survival-model predictions, or other prognostic-score summaries. MEC-updated weights therefore play a dual role as source-transport and prognostic-score balancing weights. We establish consistency, characterize a calibration-induced efficiency gain, and develop a stacked sandwich variance estimator. Simulations show that MEC-Cox can reduce bias, increase efficiency, and improve coverage through flexible machine-learning-assisted adjustment.
Causal Agent Replay: Counterfactual Attribution for LLM-Agent Failures
When an LLM agent fails -- issues a refund it should not have, calls the wrong tool, leaks data -- existing tooling answers what happened (observability) or whether it passed (evaluation), but not which step caused the failure. The obvious heuristics are wrong: the step that executes the harmful action is usually not the step that decided on it, and LLM-judge attribution is correlational and unreliable (state-of-the-art step-level accuracy on the Who&When benchmark is about 14%). We present Causal Agent Replay (CAR), which answers the question by intervention: it models an agent run as a structural causal model, applies a do-operation to a step, and re-executes the trajectory forward under the same stochastic policy, measuring the shift in the outcome distribution. We define an intervention algebra over agent steps, a single-step contrastive estimator whose point-of-commitment rule resolves a confound specific to stochastic run-forward, and a budget-bounded Monte-Carlo Shapley estimator that splits credit across interacting steps. Every effect is reported with confidence intervals. We validate against synthetic structural causal models with planted ground truth: the contrastive estimator recovers the pivotal step, and Shapley recovers a two-step interaction (0.44, 0.45, ~0; efficiency sum 0.909 versus the analytic 0.91). CAR is open source and runs on hosted or free local models.
MediEncoder: Nonlinear Representation Learning for High-Dimensional Causal Mediation Analysis
Causal mediation analysis decomposes a treatment effect into indirect pathways through mediators and direct pathways not operating through them. Modern biomedical studies often involve high-dimensional covariates and mediators that are noisy proxies for lower-dimensional latent biological processes. Existing methods typically rely on sparsity, linear factor models, or ignore the connection among variables in the learned representations, which can be restrictive when measurements are nonlinear and covariate and mediator factors are structurally dependent. We propose MediEncoder, a representation-learning framework for nonlinear high-dimensional mediation analysis. MediEncoder jointly learns low-dimensional covariate and mediator representations using a coupled encoder-decoder architecture with a cross-factor network that links treatment and covariate representations to mediator representations. The learned features are then used in a cross-fitted efficient influence function-based estimator of natural direct and indirect effects. The resulting estimator is multiply robust and asymptotically normal under suitable regularity conditions. Simulations show that MediEncoder improves estimation accuracy over competing dimension-reduction approaches, and an application to Alzheimer's Disease Neuroimaging Initiative data illustrates its utility in high-dimensional biomedical causal mediation analysis.
Does Topic Sentiment Cause Perceived Ideology? Comparing Human and LLM Annotations in Political News Articles
We ask whether topic sentiment has a causal effect on perceived political ideology, and whether the answer depends on who assigns the ideology label. Using articles from AllSides, paired with shared sentiment annotations from Llama-3.3-70b-versatile, we compare ideology labels from expert human annotators, GPT-4o-mini (baseline and finetuned), and Llama-3.3-70B. We apply Double Machine Learning (DML) and mediation analysis across all four annotation paradigms. Zero-shot LLMs regularly inflate effect sizes relative to human annotations, while fine-tuning often attenuates them back toward the human scale. Our results have implications for the use of LLM annotations as silver labels and as proxies for human judgment in downstream causal analyses: they may be reliable for recovering the presence and direction of effects on the partisan topics, but not their magnitude, leading to over- or under-prediction of some ideology given particular topics.
Human Adults and LLMs as Scientists: Who Benefits from Active Exploration?
A long-standing finding in the causal learning literature is that adults struggle to identify conjunctive causal rules, where an effect requires the simultaneous presence of multiple causes, while performing better in disjunctive settings. However, most demonstrations of this
conjunctive handicap'' rely on passive observation paradigms with limited evidence, where learners have no control over evidence generation. This paper asks whether this bias persists when adults are granted agency through active exploration. Using a modified blicket detector'' task, adult participants freely intervened to identify causal objects under conjunctive or disjunctive rule structures. We show that active exploration substantially improves adults' conjunctive causal reasoning, although conjunctive rules still require more tests to infer than disjunctive rules. We further compare human performance to a range of large language models in the same setting. While some state-of-the-art models approach human-level performance on hypothesis inference accuracy, they often exhibit less efficient exploration strategies and similar conjunctive-disjunctive performance gaps.A Pre-Registered Causal Partition of Self-Consistency Elicitation and Reward Design in RLVR
Reinforcement learning from verifiable rewards (RLVR) improves reasoning even when the reward signal is spurious -- assigning credit to the group-plurality answer rather than a ground-truth verifier. Practitioners commonly interpret naive = acc(TRUE) - acc(RANDOM) as the reward-design effect. We prove this estimand is systematically biased: it conflates self-consistency elicitation (sharpening the policy toward its modal answer via majority pseudo-reward) with genuine reward-design signal. Using a controlled tabular-GRPO simulator we derive an exact telescoping decomposition total = null + elicit + rd and measure each term across five prior-strength levels. The reward-design fraction of the naive estimator ranges from 0.139 at weak prior (ps=0.20) to 0.05 at strong prior (ps=0.80), with the elicitation term flipping sign at the self-consistency crossover. A pre-registered 2x2x2 factorial confirms non-additivity (interaction ratio 0.385; AxC effect -0.089). A points-vs-bounds pilot gate shows strong-prior regimes are point-identified while near-crossover regimes are only bounded. Re-audits of two named published results yield ELICITATION DOMINATED (elicitation share 0.98) and REWARD DESIGN DOMINATED (rd share 1.18) verdicts respectively, demonstrating the diagnostic value of the partition. We pre-commit to submit regardless of flip outcome; a non-flip is a finding of equal standing. We release a reusable one-command harness for any alignment paper to run the same audit.
Causal Longitudinal Prior-Fitted Networks for Counterfactual Outcome Prediction
Longitudinal treatment decisions from multivariate time-series data require predicting potential outcomes under future treatment sequences in the presence of time-varying confounding, heterogeneous patient dynamics, and limited domain-specific data. Existing longitudinal causal estimators typically address this problem by training a new model for each cohort or simulator. We introduce Causal Longitudinal Prior-Fitted Networks (CausalLongPFN), a prior-fitted network for time-series causal inference in longitudinal treatment-response data and zero-shot in-context counterfactual outcome prediction. The model is pretrained entirely on synthetic episodes sampled from a broad prior over temporal structural causal models, exposing it to treatment-confounder feedback, latent heterogeneity, nonlinear state evolution, delayed effects, and cumulative treatment responses. At test time, CausalLongPFN remains frozen and is used zero-shot: it conditions on support trajectories, a query history, and a planned future treatment sequence, and returns a predictive distribution over future outcomes without gradient updates or propensity-model fitting. Multi-step predictions are obtained by recursively applying the one-step predictor under the specified treatment sequence. We evaluate the model on branchable cancer, HIV, and warfarin benchmarks with ground-truth counterfactual labels, and on factual-only rolling-origin prediction in MIMIC-III ICU trajectories. CausalLongPFN is competitive with domain-trained longitudinal baselines on counterfactual benchmarks and performs strongly on factual MIMIC-III prediction, suggesting that broad synthetic causal pretraining can provide a frozen, amortized alternative for zero-shot longitudinal treatment-response prediction when repeated domain-specific training is costly or impractical.