Causal Inference

Constructing causal directed acyclic graphs (DAGs) is a core step in biomedical causal analysis, yet it remains a largely manual process. Analysts must connect study variables to prior literature, evaluate uncertain causal claims, and preserve sufficient provenance for expert review. We present EviDAG, a browser-based system for authoring causal DAGs as auditable, evidence-linked artifacts from biomedical literature. Given free-text descriptions of study concepts, EviDAG creates a reproducible literature snapshot, uses an LLM-based reasoning module to generate structured pairwise causal judgments, links literature-supported judgments to verbatim evidence excerpts, and assembles the judgments into a constraint-checked graph. Each proposed edge includes confidence estimates, provenance, and a reviewable rationale. The interface supports study specification, progress monitoring, evidence review, graph comparison, adjustment-set computation, and export. In evaluations against both compact benchmark DAGs and reference DAGs derived from published literature, EviDAG achieves high edge recall on the literature-based cohort while retaining verifiable evidence trails absent from LLM-only baselines. EviDAG thus reduces the burden of causal DAG curation while making the resulting assumptions auditable, supporting the design, analysis, and interpretation of biomedical studies.

While automated research systems promise to accelerate empirical analysis, they are prone to silent failures: instances in which analysis code executes successfully yet relies on invalid causal assumptions. We present the Artificial Intelligence (AI)-based Epidemiology Research Assistant (ARA), a framework that makes these failures visible by explicitly encoding causal design principles, study-specific assumptions, and methodological constraints. ARA integrates protocol construction, synthetic data generation, and adversarial validation into a unified pipeline. The framework translates natural language research questions into structured causal protocols and executable analysis code by first constructing a protocol and then generating synthetic datasets using Structural Causal Models (SCMs) with known ground-truth effects. This synthetic-data step can also support pipeline development when access to confidential data, such as medical data, is restricted. The generated analysis is then evaluated under controlled violations of identification assumptions. We evaluate ARA on the Automated Causal Reasoning Benchmark, assessing recovery of identification strategies, causal quantities, treatment and outcome variables, and consistency between generated code and approved protocol. Protocol construction and adversarial validation did not consistently improve numerical agreement with benchmark estimates compared with standard LLM-based generation. However, they changed the failure mode: instead of silently returning causal estimates, ARA often surfaced protocol concerns, diagnostic failures, incomplete inference, or downgraded non-causal interpretations. These findings suggest that validity-first automated science systems should be evaluated not only by answer accuracy, but also by whether they indicate when causal claims are unwarranted.

Digital twins are often used to predict how a system would respond to an intervention. In systems with feedback, a twin must reproduce an equilibrium counterfactual, and a twin developed in one domain may fail after mechanisms change. We study when these predictions can be validated and transported. For equilibrium causal games, we give conditions on the mechanisms, equilibrium selection, and intervention design under which agreement with experimental distributions identifies the counterfactual of interest. We show why agreement of means and covariances is insufficient for distributional queries. We then introduce cyclic selection diagrams and derive criteria for direct reuse and for hybrid models that combine invariant source mechanisms with target information. An impossibility result constructs systems that agree under every experiment in a finite design but disagree on the target counterfactual, showing that validation requires structural assumptions. For linear models, we derive intervention requirements that depend on the mechanisms that changed, the observation model, and graph support. When point identification fails, we characterize the remaining range of query values. We also provide statistical tests for reconstructed means and covariances and illustrate the theory in synthetic feedback systems.

Modern recommender systems are typically based on deep learning (DL) models, where a dense encoder learns representations of users and items. As a result, these systems often suffer from the black-box nature and computational complexity of the underlying models, making it difficult to systematically enhance their recommendation capabilities. To address this problem, we propose Probabilistic Residual Learning (PRL), a causal Bayesian recommendation model that models the residual between ground-truth and base predictions, enabling targeted refinement of existing systems. Specifically, PRL (1) probabilistically groups users for localized residual modeling, (2) models domain-level confounders that influence user and item representations, and (3) aggregates cluster-specific residual predictions over the confounders using do-calculus. Experiments demonstrate that our plug-and-play PRL is compatible with various base deep learning recommender systems, improving their performance while automatically discovering meaningful user clusters.

Power grids, markets, and interacting populations, settle into feedback driven equilibria observed through unknown sensors. Our Equilibrium Causal Game (ECG) joins a game to its cyclic causal model, hidden inputs, sensor map, and rules for interventions and equilibrium selection; interventions edit declared objects and recompute equilibrium. Under stated conditions, ECG-separation is sound but incomplete in our examples. Back-door/half-trek routes identify observed queries. Yet for an untouched rotationally symmetric Gaussian block, second moments determine only a source-frame rotation, across which distinct-variable effects generically change. Unknown sensing creates a separate ambiguity. In passive stable linear models without self-effects, unknown wiring and full-rank unknown sensing leave $B$ completely unidentified for $d\ge2$. Under LiNG, non-Gaussianity removes the source rotation; mechanism interventions separate sensing from interactions. With unknown support, invariant sensing, aligned responses, and well-posed single-target interventions identify $(H,B)$ up to declared equivalence. Of $d$ targets, $d-1$ suffice exactly when the sole untargeted node directly parents all others; otherwise $d$ are needed. Acquisition probes are excluded; known wiring gives no universal count. With nonlinear sensing, isotropic Gaussian source blocks admit hidden twists within and across blocks in labelled environments preserving required radial laws. Conversely, under stated positivity, informative one-block changes, rank, and irreducibility conditions, the finest independent source-block representation is identified within the stated alternative class up to block permutation and blockwise coordinate changes, but not downstream mechanisms or the sensor/interaction split. Together, these results show which causal conclusions equilibrium data support and which require targeted experiments.

We propose one-step and two-step methods for policy learning with retrieval-augmented generation (RAG). We formulate RAG-based action selection under the potential outcome framework. In the two-step method, vector search retrieves action-specific neighboring evidence in an embedding space, the generator estimates conditional expected outcomes or their contrasts, and a plug-in rule selects an action. This formulation connects action-specific vector search with nearest-neighbor matching in causal inference. We decompose the regret of the two-step method into candidate-generation regret and within-candidate choice regret, and we bound the latter using prediction-error guarantees for nearest-neighbor estimators and transformers. We evaluate the one-step method directly as a policy because its intermediate computation is unobserved.

Imitation learning enables learning a policy in an unknown environment with a latent reward signal using expert demonstrations, but it struggles when the imitator's and expert's observations are mismatched and unobserved confounders are present in expert demonstrations. By identifying appropriate adjustment sets via the sequential $π$-backdoor criterion, causal imitation learning (CIL) provides a framework for approximating the expert's policy from confounded data. However, existing CIL methods, Causal Behavioral Cloning (Causal BC) and Causal Generative Adversarial Imitation Learning (Causal GAIL), are designed for short-horizon, low-dimensional settings. When applied to continuous control tasks with long horizons and high-dimensional state-action spaces, these methods exhibit poor performance: Causal BC suffers from compounding errors, Causal GAIL is unstable and sample-inefficient, and sequential $π$-backdoor adjustment becomes impractical. We introduce Causal Soft Q Imitation Learning (SQIL) and Causal Inverse soft-Q Learning (IQ-Learn), two off-policy causal imitation learning algorithms that combine the causal adjustment framework with state-of-the-art inverse reinforcement learning objectives. Both algorithms operate on causally-adjusted state representations produced by an efficient approximation of the sequential $π$-backdoor criterion, exploiting the causal structure of continuous control environments to reduce the full-horizon adjustment to a fixed-size sliding window. We evaluate all methods in a suite of confounded environments and find that Causal SQIL and Causal IQ-Learn substantially outperform prior CIL algorithms on long-horizon tasks, sometimes surpassing the expert, whereas all causally unaware imitation methods fail to learn meaningful behavior.

We study causal inference under outcome interference for sequential, observational settings. Specifically, we consider settings where the binary outcomes over N units are Markovian across T time steps. At each time step, the outcomes of N units have dependencies captured through an Ising model; each outcome is also impacted through an external field capturing the effects of its treatment as well as latent confounders. Similar to panel data literature, these latent confounders are modeled to have a low-rank factor structure. Our data is a single sample from this high-dimensional distribution. To estimate causal quantities of interest, we provide a computationally efficient method based on Maximum Pseudo-Likelihood Estimation (MPLE) for learning the model parameters. Under mild assumptions, we establish non-asymptotic consistency for parameter estimation and show this translates to faithful estimation of causal quantities of interest after sampling from the learned model. We demonstrate the efficacy of the method through synthetic experiments as well as a real-world case-study investigating causal effects of vaccine rates on COVID-19 death rates within US counties nationwide.

This paper addresses Carl Hempel's longstanding problem of statistical ambiguity in inductive-statistical inference, in which contradictory predictions are derived from statistical laws. To avoid such predictions, Carl Hempel proposed the Requirement of Maximal Specificity (RMS) for the statistical laws used in the inference. An analysis of the RMS refinements made by Wesley Salmon, Alberto Coffa, and James Fetzer led to the following definition of maximally specific statistical laws: "the lawlike premises of an adequate explanation must specify all and only those properties whose presence or absence made a difference to the occurrence of its explanandum-phenomenon." However, there was no proof of a solution to the statistical ambiguity problem based on this definition. We use Nancy Cartwright's definition of causes that raise probabilities across background contexts, and then introduce the concept of Causal Rules. Then we define a special semantic probabilistic inference procedure that incrementally refines these causal rules by incorporating all statistically relevant information. This procedure yields Maximally Specific Causal Relationships (MSCRs), for which we prove (Theorem 1) that predictions derived from them are consistent. This resolves the statistical ambiguity problem. The semantic probabilistic inference procedure provides a probabilistic causal learning system, which may be used in such new areas as Causal AI and Causal Machine Learning. They fundamentally explore causal inference as a tool for understanding cause-and-effect relationships within complex systems. Properties similar to RMS remain under discussion. Several notions related to RMS are considered: invariant feature learning, invariant causal prediction, and spurious association.

Causal inference using front door intervention and multi-instance learning (MIL) has advanced the analysis of Whole Slide Images (WSI) in digital pathology. These methods adjust feature distributions of subtle evidence sub-images to correctly associate them with WSI-level diagnoses. We propose and prove 2 hypotheses for evaluating such methods: 1) Causal inference MIL introduces an independent classification channel that effectively completes WSI classification; 2) Greater difference between features extracted by the new and baseline channels increases effectiveness in eliminating false correlations. This hypothesis describes the core of causal inference MILs: overlaying parallel, independent channels to eliminate false associations between WSI-level diagnostic and non-diagnostic evidence sub-images by increasing deep feature diversity. Based on these hypotheses, we evaluated several causal inference MILs on breast cancer and non-small cell lung cancer datasets. This hypothesis provides a new theoretical perspective for applying causal inference to WSI analysis.

Workload-based differentially private (DP) synthetic data methods privately measure aggregate queries and post-process the noisy answers into synthetic records. Generic workloads can achieve strong distributional fidelity, but causal estimands such as the average treatment effect (ATE) depend on treatment-arm balance and outcome moments that generic marginals need not preserve. We propose causal workloads: DP query sets designed around the orthogonal moments used by doubly robust causal estimators. The released workload can be used directly by stable moment-map estimators or reconstructed by maximum-entropy calibration into reusable synthetic data; our theory decomposes ATE error into sampling, privacy, workload-approximation, Monte Carlo, and calibration terms. We also introduce Causal-AIM, an adaptive workload selector, and a noise-aware multiple-imputation (NA+MI) procedure for confidence intervals from DP synthetic data. Because the workload is released once, the same DP synthetic table can support ATE, ATT, and subgroup analyses without additional privacy spending. Empirically, causal workloads are most useful at strict privacy budgets and for calibrated uncertainty, while generic workloads often retain an advantage for point RMSE as privacy relaxes. The broader lesson is a tradeoff: distributional fidelity can help point accuracy, but valid causal inference requires preserving causal moments and propagating DP noise rather than treating synthetic rows as real.

Optimizer experiments observe responses to algorithmic configurations without uniquely revealing hidden mechanisms. We develop a causal optimizer interaction calculus that separates pathwise realization, Mobius decomposition, and experimental identification. Under a fixed innovation coupling, every finite-horizon innovation-driven optimizer admits a behaviorally minimal pathwise realization. For any finite effect support and intervention design, an incidence operator gives the complete observational gauge, exact identifiability, sharp quotient stability, held-out predictions, and exact noiseless configuration complexity. Smooth hidden relaxation generates interactions through inverse hidden-state stiffness. Building on this structural law, we prove an observable-readout transfer theorem: arbitrary smooth update or trace readouts inherit an explicit five-term interaction through first and second hidden responses. Unlike the reduced optimal value, a general readout has no universal interaction sign. Its Boolean effects remain exact integrals of continuous interaction curvature and can therefore be identified by factorial interventions. We also derive Gaussian quotient minimax risk, exact confidence sets and tests, misspecification decomposition, certified downstream decisions, and optimal replication. A controlled real-data experiment on a 65-dimensional strongly convex logistic model validates the complete reduced-value chain. Boolean effects and independently integrated curvature agree within 4.21e-11, while nine held-out continuous intensities agree within 8.88e-13. Gaussian campaigns attain the predicted coverage and power, and 4,500 real-minibatch observations reject an order-two interaction model. Neural trace audits provide complementary evidence that the declared response classes remain informative in nonconvex training.

Personalized incentive allocation is vital for e-commerce, where uplift modeling is the standard for estimating Individual Treatment Effects (ITE). However, traditional models often fail in complex multi-seller environments with violations of the Stable Unit Treatment Value Assumption (SUTVA). We identify two critical challenges: Seller-level Cannibalization, where incentives shift expenditure between shops without growing the platform, and Incentive-level Cannibalization, where organic conversions or alternative rewards introduce significant noise into incrementality estimation. In this paper, we propose CanniUplift, a unified framework to mitigate these dual-source cannibalization effects. Specifically, we design Platform-level Global Alignment (PGA) to capture cross-shop substitution through global GMV consistency constraints. To tackle incentive-driven noise, we introduce Redemption-based Decomposition Denoising (RDD), which uses redemption behavior to decompose treated outcomes and reduce attribution noise within an entire-space framework. Furthermore, a Treat-Attention mechanism is designed to model intricate interactions between users' historical behaviors and current treatment options. Extensive experiments on both synthetic and large-scale industrial datasets demonstrate that CanniUplift significantly outperforms state-of-the-art baselines. Ablation studies confirm that the integration of PGA and RDD consistently improves wAUUC and wQINI. Successfully deployed online, our framework achieved a 4.08% relative increase in platform-wide incremental GMV (Delta GMV) over the production baseline and improved ROI in online A/B tests, proving effective in driving global platform growth.

Diabetic retinopathy (DR) is a local retinal lesion process and a visible manifestation of systemic microvascular injury. Modern retinal AI can grade images accurately, but often leaves unanswered how local lesion evidence, retinal vascular structure, and systemic disease pathways are connected. This paper introduces \emph{Causal-RetiGraph}, a compact biomedical informatics framework that links retinal graph phenotypes with NHANES-anchored pathway modelling. The retinal-image fold constructs an interpretable $X1234$ phenotype from vessel maps, lesion evidence, image embeddings, and AutoMorph biomarkers through spatial $X_{12}$ and Jacobian $X_{34}$ branches. The NHANES fold models systemic exposures, covariates, a same-subject retinal mediator family $R^*$, and downstream outcome families. $X1234$ is used for retinal support and pathway prioritisation, while $R^*$ is used for participant-level pathway summaries. On the retinal fold, $X1234$ achieves 0.9055 binary DR accuracy and 0.9711 AUROC, with graded DR QWK of 0.8312. The results show that lesion and biomarker streams improve contextual retinal representation under scarce and imbalanced data. In NHANES, HbA1c, urine albumin, pulse pressure, fasting glucose, and systolic blood pressure are the strongest binary DR anchors. Participant-level pathway analysis identifies glycaemic--renal and glycaemic--haemodynamic pathways as the clearest mediator-style signals. These results suggest that retinal graph phenotypes can help prioritise systemic pathways in DR while preserving the distinction between image-derived support and same-subject mediation.

Scientists often seek to draw causal inferences from structured data that is not independently and identically distributed, such as spatial data, network data, or molecular data. We develop geometric causal models (GCMs), a framework for causal inference from dependent data that exploits underlying symmetries of the data generating process. For example, in spatial data, we consider processes that are symmetric under translations, or in graph data, symmetric under permutations of the nodes. We show how symmetries, formalized with group theory, can enable causal identification and estimation. We deploy ergodic theory for amenable groups to establish identification, and combine geometric deep learning with scalable Bayesian inference for estimation. We recover i.i.d. causal models and do-calculus when the data is a sequence and the symmetry is permutation equivariance, and find novel types of causal models when we use alternate structures and symmetries. As an example, we construct a causal model that satisfies the symmetries of DNA. This GCM enables new estimators for the effects of genetic variation, combining deep functional genomics models to describe outcomes and DNA language models to describe propensities. We illustrate on semisynthetic data.

This paper studies the problem of identifying the treatment that maximizes the expected natural direct potential outcome (NDPO), which captures the potential outcome of an intervention while excluding the pathway transmitted through a mediator that researchers may wish to remove from evaluation. We first establish population-level identification of the expected NDPO in a causal bandit setting using observable interventional distributions. We then develop a fixed-confidence best-arm identification (BAI) algorithm based on the Track-and-Stop (TaS) framework, employing a cutting-set method to solve the resulting semi-infinite optimization problem. The proposed algorithm achieves sample-efficient identification with a high-probability correctness guarantee. We prove that it satisfies $δ$-correctness and asymptotic optimality. Finally, we validate the approach through empirical evaluations on a large-scale real-world advertising dataset (IPinYou).

Estimating heterogeneous treatment effects (CATE) requires simultaneously detecting effect modification and quantifying estimation uncertainty. Existing tree-based methods make an uneasy trade-off: significance-based approaches (Radcliffe and Surry 2011) identify subgroup interactions directly but lack valid inference; honest causal trees (Athey and Imbens 2016) deliver nominal confidence interval coverage but use outcome-agnostic splitting criteria that sacrifice interaction sensitivity. We introduce a hybrid algorithm that fuses significance-based splitting with honest sample-splitting and cross-validation. Our splitting criterion uses the squared $t$-statistic for the treatment $\times$ side interaction ($t^2$), which is shown to be directly aligned with the honest $\text{EMSE}_τ$ criterion when the interaction is strong. Post-hoc honest cross-validation selects the cost-complexity penalty, giving a single principled estimator with nominal CI coverage at the leaf level. For forests, we retain bootstrap count vectors to enable an infinitesimal jackknife (IJ) variance estimate of Monte-Carlo convergence rather than formal pointwise inference. On the three synthetic designs from (Athey and Imbens 2016) the single tree achieves approximately 90% leaf-average CI coverage at the 90% nominal level across all three designs (200 replications each); on the Criteo, Hillstrom and Starbucks uplift datasets we match Qini coefficient performance of S-, T-learner and GRF baselines. An open-source Python package with reproducible seeds, sklearn-compatible API, and full test coverage accompanies this work (https://codeberg.org/hadjipantelis/rattus).

Background: Growing individual case safety report (ICSR) volumes have intensified demand for scalable automated causality assessment. Large Language Models (LLMs) show promise, yet performance on clinically demanding tasks remains suboptimal and inference-time hyperparameter optimization has not been investigated. Objective: To develop a Gaussian Process (GP)-compatible optimization objective and investigate whether temperature optimization improves LLM-expert agreement on Naranjo causality assessment of FAERS ICSRs. Methods: Expert causality assessments were performed on 723 stratified FAERS cases. OpenAI's GPT-5.2 was evaluated using chain-of-thought (CoT) prompting. Four composite metrics were developed: Weighted Cosine Similarity (WCS), Information-Weighted Agreement Score (IWAS), Entropy-Weighted Agreement and Cosine Similarity Score (EWACS), and Consensus-Weighted Cosine Similarity (CWCS) and Bayesian optimization using a GP surrogate with Probability of Improvement (PoI) acquisition was applied across temperature [0, 2]. Results: GPT-5.2 outperformed prior biomedical LLMs at baseline (T = 0), achieving 74.1% agreement on question 5 and 65.4% on question 10 of Naranjo algorithm. Entropy analysis identified these as the sole informative optimization targets. Temperature showed no systematic population-level effect (\b{eta} = 0.002, p = 0.959). EWACS-guided Bayesian optimization improved causality classification agreement from 45.0% to 72.0% (+27 pp), with the largest gain in Doubtful cases (+42.9 pp). Conclusion: EWACS was identified as the optimal GP-compatible metric. The absence of a universal temperature optimum indicates LLM performance is driven primarily by ICSR content, yet case-specific temperature selection produced meaningful improvements, supporting temperature optimization for LLM-assisted pharmacovigilance.

We propose \textbf{CaSPECT}, a causal spectral clustering framework for discovering causally homogeneous subgroups from observational data. Rather than clustering in covariate space, CaSPECT defines similarity through the topology of a learned directed acyclic graph (DAG); a bootstrap-stabilised PC algorithm recovers the causal skeleton; a novel \emph{Orientation Validation Score} (OVS) combines PC bootstrap evidence with DirectLiNGAM to orient edges robustly; directed edges are weighted by backdoor-identified average treatment effects estimated via OLS or double machine learning. Chung's directed Laplacian provides a spectral embedding in which individuals close together share the same causal propagation pathways. We establish almost-sure consistency of the full pipeline and validate the method through a controlled simulation study and on LaLonde CPS1, IHDP, and 401(k) datasets, where CaSPECT recovers a positive and statistically significant treatment effect within the causally comparable subpopulation and corrects for severe confounding without requiring a pre-specified propensity score model.

Multicollinearity is a long lasting challenge in observational causal inference, especially in regressions -- highly correlated independent variables make it hard to isolate their individual impacts on outcomes of interest. While common solutions such as shrinkage estimators and principal component regressions are helpful in prediction problems, a crucial limitation hinders their applicability to causal inference problems -- they cannot provide the original causal relationships. To fill the gap, we present an innovative and intuitive solution, by employing hierarchical clustering to aggregate data in a way that effectively alleviates collinearity. This method is generally applicable to causal problems featuring multicollinearity. We use a marketing application to demonstrate how and why it works. Expenditures on different advertising channels often exhibit correlations, making it exceedingly difficult to separately measure their impact. Many previous studies proposed to leverage granular cross-sectional data for better identification but, to our knowledge, none explicitly addressed multicollinearity, which undermines causal identification even with granular data. We propose to hierarchically cluster geographic units based on marketing spend correlation to reduce collinearity, and to implement a Bayesian Marketing Mix Model with cluster-level data. Such clustering happens in two steps -- we first normalize and demean geo-level data to establish a common scale and to eliminate the common trends; we then calculate pairwise distance to summarize marketing spend correlation between geos and cluster the ones with moderate to strong correlation. Both descriptive evidence and regression analysis affirm that such hierarchical clustering effectively mitigates collinearity and facilitates the separate identification of the impact of different marketing channels.

We propose doubly robust adaptive conformal inference (DR-ACI), which constructs prediction intervals for doubly robust pseudo-outcomes under temporal dependence.

We consider sparse multivariate stochastic systems that evolve in continuous time according to a causal mechanism and present methodology to recover the system's time-infinitesimal transition mechanism from mere cross-sectional data. This observational paradigm is motivated by applications such as gene expression analysis, where destructive experimental techniques may only allow recording data once over a cell's lifetime. Precisely, we assume the system follows a time-homogeneous diffusion process that has reached an equilibrium distribution at observation time. Further, we assume the causal mechanism is fully described by the diffusion drift, is acyclic, and its causal structure graph is known. In this setting, we prove that the full causal mechanism, i.e., the drift function, can be non-parametrically identified under a weak non-explosion criterion. We derive a non-parametric kernel estimator for this challenging inverse problem and prove its consistency. Moreover, we propose a cross-validation scheme for hyperparameter tuning, illustrate the behavior of our estimator in simulations, and we discuss connections with irreversible generative diffusion models and low-frequency sampled data.

Probabilistic model checking for Markov decision processes (MDPs) provides quantitative guarantees, but often offers limited insight into why undesired outcomes occur. Probability-raising (PR) causality addresses this by identifying states whose visitation increases the probability of reaching designated states. Existing PR-cause identification methods, however, use MDP modifications not well-suited for learning: the gap between conditional and unconditional reachability probabilities can be hard to detect from transition samples, and construction requires reachability probabilities of the MDP, which are unavailable when transition probabilities are unknown. We study unknown MDPs and propose a learning approach with probabilistic guarantees for PR-cause identification. Our key ingredient is a restart-based MDP modification that reduces PR-cause checking to two conditional reachability queries without using reachability values of the original MDP. We prove correctness, establish sample-complexity bounds, and develop an anytime learning-and-checking algorithm based on two-sided value iteration that progressively classifies states as causal, non-causal, or undecided. Experiments on two benchmarks demonstrate reliable and fast identification of PR causes.

Lifted inference exploits indistinguishabilities in probabilistic graphical models by using a representative for indistinguishable objects, thereby speeding up query answering while maintaining exact answers. In this article, we show how lifting can be applied to efficiently compute causal effects in relational domains. More specifically, we introduce parametric causal factor graphs (PCFGs) to incorporate causal knowledge in lifted models and give a formal semantics of interventions therein. We further present the Lifted Causal Inference (LCI) algorithm to compute causal effects on a lifted level, thereby drastically speeding up causal inference compared to propositional inference, e.g., in causal Bayesian networks. In addition, we present partially directed parametric causal factor graphs (PD-PCFGs) as a generalisation of PCFGs to handle partial causal knowledge and extend LCI to perform lifted causal inference in a PD-PCFG, thereby extending the applicability of lifted causal inference to a broader range of models requiring less prior knowledge about causal relationships.

Activation patching is the primary tool in mechanistic interpretability. It attributes causal responsibility for a model behavior to each of its individual components by estimating its natural indirect effect (NIE). Re-deriving the activation patching estimand from causal mediation analysis, we find that the NIE does not solely capture the causal effect through the specific component. It also contains interaction effects (INT) that measure how much the component's causal effect itself depends on the state of other components in the model. A natural response may be to try to eliminate INT by adjusting the estimator or unit of analysis, but each of these potential remedies has predictable failure modes. We demonstrate these failure modes in the GPT-2 IOI circuit; components whose causal importance is conditional on the state of other components are either invisible or artificially inflated, and INT variance explains the previously documented instability of faithfulness scores. We prove that INT scales with the distance between clean and patched component activations, is negligible when the model is locally affine, and decomposes combinatorially into pairwise and higher-order group interactions. Despite its inevitability, INT is not a nuisance to be eliminated, but rather a diagnostic for interpretability studies. Its individual and group-level magnitude and sign signal when causal conclusions are prompt-dependent, and when greedy NIE-based component ranking will miss mechanisms only discoverable through combinatorial search.

Uplift modeling, crucial for estimating individual treatment effects (ITE), faces dual challenges: flexibly leveraging inter-group similarity to enhance discriminative power and debiasing under unobserved confounding scenarios. In this paper, we propose the Cross-Head Attention Uplift Network (CHAUN) and Robust Adversarial Inverse Propensity Score (RA-IPS) method to address these limitations. CHAUN employs shared feature embeddings and cross-head attention mechanisms to dynamically integrate treatment-specific and control-specific representations, enhancing inter-group correlation modeling. Theoretically, we prove that access to the true propensity scores ensures ITE identifiability even with unobserved confounders. For practical scenarios lacking true propensity scores, RA-IPS adversarially optimizes propensity weights within constrained uncertainty sets to mitigate bias from unobserved variables. Experiments on public datasets (CRITEO-UPLIFT, LAZADA) and a production e-commerce dataset demonstrate CHAUN's superiority over state-of-the-art uplift models, achieving relative improvements of up to 25.6% in QINI scores. RA-IPS further enhances robustness, outperforming standard IPS by 5.4% under unobserved confounding. The results validate the effectiveness of our proposed methods in real-world causal inference tasks.

We introduce TabPFN-CFM, a causal foundation model that can handle multiple causal problems. TabPFN-CFM predicts both causal structure and outcomes from observational data, supports queries on all three levels of Pearl's Causal Hierarchy and uses known graph structure when available to improve predictions. TabPFN-CFM is trained on synthetic datasets, and generalises to real datasets, demonstrating improved performance over both structural and outcome prediction baselines.

This paper introduces a categorical account of infinitesimal causality in Frobenius Markov categories equipped with tangent-bundle semantics. IDC captures the infinitesimal layer in which interventions act as tangent deformations of copy/discard structure. Two distinct Frobenius structures interact: (1) the categorical Frobenius algebra on classical variables encoding copying, comparing, and discarding; and (2) the geometric Frobenius integrability condition, namely involutive closure of the intervention distribution, distinct from the algebraic Frobenius structure. Categorical causal sufficiency is defined as the compatibility of these two notions. A key observation is that, for structural causal models, infinitesimal causality is most naturally formulated in the slice of deterministic mechanisms over exogenous variables, with visible stochastic kernels obtained only after pushforward. Interventions are tangent vectors that deform the Frobenius copy/discard operations; their Lie brackets measure whether this deformation preserves classical information-flow structure. Pearl's do-calculus is used as a guiding example of intervention identities: ignoring irrelevant interventions corresponds to counit invariance, action/observation exchange to coproduct compatibility with pushforward, and independence to involutive bracket closure of the visible intervention distribution.

Learning causal models from fragmented biomedical data is challenging because clinical, molecular, and imaging variables are often incomplete or not jointly observed. We propose RetiSEM, a domain-constrained structural equation modelling (SEM) framework for causal graph recovery and mediation analysis under limited multimodal resources. This proposed work organises variables into biologically informed blocks, applies forbidden-edge constraints, and decomposes pathway-level effects into TE, NDE, and NIE components. We evaluate RetiSEM across ten synthetic benchmark scenarios that vary in dimensionality, nonlinearity, causal depth, and pathway structure, together with a fragmented real-world setting that combines NHANES clinical variables with externally derived retinal representations. This approach achieves lower structural error and higher causal accuracy than unconstrained baselines across the synthetic benchmarks. In the real-data analysis, retinal variables behave mainly as downstream biomarker-like indicators, with smaller but detectable indirect effects. These findings support our strategy as an interpretable framework for testing structured causal hypotheses in limited-resource biomedical AI. The code and resources for this work are publicly available at: https://github.com/Inamullah-Colab/ReitSEM.

Causal inference provides a set of principles and tools that allow one to combine data and knowledge about an environment to reason with questions of counterfactual nature, i.e., what would have happened had reality been different, even when no data of this unrealized reality is currently available. Reinforcement learning provides methods to learn a policy that optimizes a specific measure (e.g., reward, regret) when the agent is deployed in an environment and pursues an exploratory, trial-and-error approach. These two disciplines have evolved independently and with virtually no interaction between them. We note that they operate over different aspects of the same building block, counterfactual relations, which makes them umbilically connected. Based on these observations, novel learning opportunities arise when this connection is explicitly acknowledged and mathematized. To realize this potential, we note that any environment where the RL agent is deployed can be decomposed as a collection of autonomous mechanisms with different causal invariances, parsimoniously modeled as a structural causal model; any standard RL setting implicitly encodes such a model. This formalization allows us to put under a unifying treatment different modes of learning, including online, off-policy, and causal calculus learning, which appear unrelated in the literature. However, these modalities are not exhaustive: we introduce several natural and pervasive classes of learning settings that entail novel dimensions of analysis. Specifically, we introduce and discuss through causal lenses generalized policy learning, where to intervene, imitation learning, and counterfactual learning. These tasks lead to a broader view of counterfactual learning and suggest great potential for studying causal inference and reinforcement learning side by side, which we call causal reinforcement learning (CRL).