ICML 2025 Papers

Causal estimands can vary significantly depending on the relationship between outcomes in treatment and control groups, leading to wide partial identification (PI) intervals that impede decision making. Incorporating covariates can substantially tighten these bounds, but requires determining the range of PI over probability models consistent with the joint distributions of observed covariates and outcomes in treatment and control groups. This problem is known to be equivalent to a conditional optimal transport (COT) optimization task, which is more challenging than standard optimal transport (OT) due to the additional conditioning constraints. In this work, we study a tight relaxation of COT that effectively reduces it to standard OT, leveraging its well-established computational and theoretical foundations. Our relaxation incorporates covariate information and ensures narrower PI intervals for any value of the penalty parameter, while becoming asymptotically exact as a penalty increases to infinity. This approach preserves the benefits of covariate adjustment in PI and results in a data-driven estimator for the PI set that is easy to implement using existing OT packages. We analyze the convergence rate of our estimator and demonstrate the effectiveness of our approach through extensive simulations, highlighting its practical use and superior performance compared to existing methods.

Federated causal structure learning aims to infer causal relationships from data stored on individual clients, with privacy concerns. Most existing methods assume identical variable sets across clients and present federated strategies for aggregating local updates. However, in practice, clients often observe overlapping but non-identical variable sets, and non-overlapping variables may introduce spurious dependencies. Moreover, existing strategies typically reflect only the overall quality of local graphs, ignoring the varying importance of relationships within each graph. In this paper, we study federated causal structure learning with non-identical variable sets, aiming to design an effective strategy for aggregating “correct” and “good” (non-)causal relationships across distributed datasets. Specifically, we first develop theories for detecting spurious dependencies, examining whether the learned relationships are “correct” or not. Furthermore, we define stable relationships as those that are both “correct” and “good” across multiple graphs, and finally design a two-level priority selection strategy for aggregating local updates, obtaining a global causal graph over the integrated variables. Experimental results on synthetic, benchmark and real-world data demonstrate the effectiveness of our method.

In experimental causal inference, we distinguish between two sources of uncertainty: design uncertainty, due to the treatment assignment mechanism, and sampling uncertainty, when the sample is drawn from a super-population. This distinction matters in settings with small fixed samples and heterogeneous treatment effects, as in geographical experiments. The standard bootstrap procedure most often used by practitioners primarily estimates sampling uncertainty, and the causal bootstrap procedure, which accounts for design uncertainty, was developed for the completely randomized design and the difference-in-means estimator, whereas non-standard designs and estimators are often used in these low-power regimes. We address this gap by proposing an integer program which computes numerically the worst-case copula used as an input to the causal bootstrap method, in a wide range of settings. Specifically, we prove the asymptotic validity of our approach for unconfounded, conditionally unconfounded, and and individualistic with bounded confoundedness assignments, as well as generalizing to any linear-in-treatment and quadratic-in-treatment estimators. We demonstrate the refined confidence intervals achieved through simulations of small geographical experiments.

Tailoring treatments to individual needs is a central goal in fields such as medicine. A key step toward this goal is estimating Heterogeneous Treatment Effects (HTE)—the way treatments impact different subgroups. While crucial, HTE estimation is challenging with survival data, where time until an event (e.g., death) is key. Existing methods often assume complete observation, an assumption violated in survival data due to right-censoring, leading to bias and inefficiency. Cui et al. (2023) proposed a doubly-robust method for HTE estimation in survival data under no hidden confounders, combining a causal survival forest with an augmented inverse-censoring weighting estimator. However, we find it struggles under heavy censoring, which is common in rare-outcome problems such as Amyotrophic lateral sclerosis (ALS). Moreover, most current methods cannot handle instrumental variables, which are a crucial tool in the causal inference arsenal. We introduce Multiple Imputation for Survival Treatment Response (MISTR), a novel, general, and non-parametric method for estimating HTE in survival data. MISTR uses recursively imputed survival trees to handle censoring without directly modeling the censoring mechanism. Through extensive simulations and analysis of two real-world datasets—the AIDS Clinical Trials Group Protocol 175 and the Illinois unemployment dataset we show that MISTR outperforms prior methods under heavy censoring in the no-hidden-confounders setting, and extends to the instrumental variable setting. To our knowledge, MISTR is the first non-parametric approach for HTE estimation with unobserved confounders via instrumental variables.

Interpretability research now offers a variety of techniques for identifying abstract internal mechanisms in neural networks. Can such techniques be used to predict how models will behave on out-of-distribution examples? In this work, we provide a positive answer to this question. Through a diverse set of language modeling tasks—including symbol manipulation, knowledge retrieval, and instruction following—we show that the most robust features for correctness prediction are those that play a distinctive causal role in the model’s behavior. Specifically, we propose two methods that leverage causal mechanisms to predict the correctness of model outputs: counterfactual simulation (checking whether key causal variables are realized) and value probing (using the values of those variables to make predictions). Both achieve high AUC-ROC in distribution and outperform methods that rely on causal-agnostic features in out-of-distribution settings, where predicting model behaviors is more crucial. Our work thus highlights a novel and significant application for internal causal analysis of language models.

We tackle the problem of identifying whether a variable is the cause of a specified target using observational data. State-of-the-art causal learning algorithms that handle latent variables typically rely on identifying the global causal structure, often represented as a partial ancestral graph (PAG), to infer causal relationships. Although effective, these approaches are often redundant and computationally expensive when the focus is limited to a specific causal relationship. In this work, we introduce novel local characterizations that are necessary and sufficient for various types of causal relationships between two variables, enabling us to bypass the need for global structure learning. Leveraging these local insights, we develop efficient and fully localized algorithms that accurately identify causal relationships from observational data. We theoretically demonstrate the soundness and completeness of our approach. Extensive experiments on benchmark networks and real-world datasets further validate the effectiveness and efficiency of our method.

Causal machine learning has the potential to revolutionize decision-making by combining the predictive power of machine learning algorithms with the theory of causal inference. However, these methods remain underutilized by the broader machine learning community, in part because current empirical evaluations do not permit assessment of their reliability and robustness, undermining their practical utility. Specifically, one of the principal criticisms made by the community is the extensive use of synthetic experiments. We argue, on the contrary, that **synthetic experiments are essential and necessary to precisely assess and understand the capabilities of causal machine learning methods**. To substantiate our position, we critically review the current evaluation practices, spotlight their shortcomings, and propose a set of principles for conducting rigorous empirical analyses with synthetic data. Adopting the proposed principles will enable comprehensive evaluations that build trust in causal machine learning methods, driving their broader adoption and impactful real-world use.

Identifying variables responsible for changes to a biological system enables applications in drug target discovery and cell engineering. Given a pair of observational and interventional datasets, the goal is to isolate the subset of observed variables that were the targets of the intervention. Directly applying causal discovery algorithms is challenging: the data may contain thousands of variables with as few as tens of samples per intervention, and biological systems do not adhere to classical causality assumptions. We propose a causality-inspired approach to address this practical setting. First, we infer noisy causal graphs from the observational and interventional data. Then, we learn to map the differences between these graphs, along with additional statistical features, to sets of variables that were intervened upon. Both modules are jointly trained in a supervised framework, on simulated and real data that reflect the nature of biological interventions. This approach consistently outperforms baselines for perturbation modeling on seven single-cell transcriptomics datasets. We also demonstrate significant improvements over current causal discovery methods for predicting soft and hard intervention targets across a variety of synthetic data.

Despite the success of Large Language Models (LLMs) across various fields, their potential to generate untruthful and harmful responses poses significant risks, particularly in critical applications. This highlights the urgent need for systematic methods to detect and prevent such misbehavior. While existing approaches target specific issues such as harmful responses, this work introduces LLMScan, an innovative LLM monitoring technique based on causality analysis, offering a comprehensive solution. LLMScan systematically monitors the inner workings of an LLM through the lens of causal inference, operating on the premise that the LLM's `brain' behaves differently when generating harmful or untruthful responses. By analyzing the causal contributions of the LLM's input tokens and transformer layers, LLMScan effectively detects misbehavior. Extensive experiments across various tasks and models reveal clear distinctions in the causal distributions between normal behavior and misbehavior, enabling the development of accurate, lightweight detectors for a variety of misbehavior detection tasks.

Previous studies have extensively addressed the attribution problem for binary outcome variables. However, in many practical scenarios, the outcome variable is continuous, and simply binarizing it may result in information loss or biased conclusions. To address this issue, we propose a series of posterior causal estimands for retrospectively evaluating multiple correlated causes from a continuous outcome. These estimands include posterior intervention effects, posterior total causal effects, and posterior natural direct effects. Under assumptions of sequential ignorability, monotonicity, and perfect positive rank, we show that the posterior causal estimands of interest are identifiable and present the corresponding identification equations. We also provide a simple but effective estimation procedure and establish asymptotic properties of the proposed estimators. An artificial hypertension example and a real developmental toxicity dataset are employed to illustrate our method.

Through recognizing causal subgraphs, causal graph learning (CGL) has risen to be a promising approach for improving the generalizability of graph neural networks under out-of-distribution (OOD) scenarios. However, the empirical successes of CGL techniques are mostly exemplified in classification settings, while regression tasks, a more challenging setting in graph learning, are overlooked. We thus devote this work to tackling causal graph regression (CGR); to this end we reshape the processing of confounding effects in existing CGL studies, which mainly deal with classification. Specifically, we reflect on the predictive power of confounders in graph-level regression, and generalize classification-specific causal intervention techniques to regression through a lens of contrastive learning. Extensive experiments on graph OOD benchmarks validate the efficacy of our proposals for CGR. The model implementation and the code are provided on https://github.com/causal-graph/CGR.

Structural causal models (SCMs) allow us to investigate complex systems at multiple levels of resolution. The causal abstraction (CA) framework formalizes the mapping between high- and low-level SCMs. We address CA learning in a challenging and realistic setting, where SCMs are inaccessible, interventional data is unavailable, and sample data is misaligned. A key principle of our framework is *semantic embedding*, formalized as the high-level distribution lying on a subspace of the low-level one. This principle naturally links linear CA to the geometry of the *Stiefel manifold*. We present a category-theoretic approach to SCMs that enables the learning of a CA by finding a morphism between the low- and high-level probability measures, adhering to the semantic embedding principle. Consequently, we formulate a general CA learning problem. As an application, we solve the latter problem for linear CA; considering Gaussian measures and the Kullback-Leibler divergence as an objective. Given the nonconvexity of the learning task, we develop three algorithms building upon existing paradigms for Riemannian optimization. We demonstrate that the proposed methods succeed on both synthetic and real-world brain data with different degrees of prior information about the structure of CA.

The Risk Difference (RD), an absolute measure of effect, is widely used and well-studied in both randomized controlled trials (RCTs) and observational studies. Complementary to the RD, the Risk Ratio (RR), as a relative measure, is critical for a comprehensive understanding of intervention effects: RD can downplay small absolute changes, while RR can highlight them. Despite its significance, the theoretical study of RR has received less attention, particularly in observational settings. This paper addresses this gap by tackling the estimation of RR in observational data. We propose several RR estimators and establish their theoretical properties, including asymptotic normality and confidence intervals. Through analyses on simulated and real-world datasets, we evaluate the performance of these estimators in terms of bias, efficiency, and robustness to generative data models. We also examine the coverage and length of the associated confidence intervals. Due to the non-linear nature of RR, influence function theory yields two distinct efficient estimators with different convergence assumptions. Based on theoretical and empirical insights, we recommend, among all estimators, one of the two doubly-robust estimators, which, intriguingly, challenges conventional expectations.

Machine learning (ML) systems are utilized in critical sectors such as healthcare, law enforcement, and finance, but often rely on historical data that contains demographic biases, leading to decisions that perpetuate or intensify existing inequalities. Causal and counterfactual fairness provide a transparent, human-in-the-loop framework to mitigate algorithmic discrimination, aligning closely with legal doctrines of direct and indirect discrimination. However, current causal fairness frameworks hold a key limitation in that they assume prior knowledge of the correct causal model, restricting their applicability in complex fairness scenarios where causal models are unknown or difficult to identify. To bridge this gap, we propose FairPFN, a tabular foundation model pre-trained on synthetic causal fairness data to identify and mitigate the causal effects of protected attributes in its predictions. FairPFN's key contribution is that it requires no knowledge of the causal model and demonstrates strong performance across a diverse set of hand-crafted and real-world causal scenarios relative to robust baseline methods. FairPFN paves the way for a promising direction for future research, making causal fairness more accessible to a wider variety of complex fairness problems.

Causal machine learning (ML) promises to provide powerful tools for estimating individual treatment effects. While causal methods have placed some emphasis on heterogeneity in treatment response, it is of paramount importance to clarify the nature of this heterogeneity, by highlighting which variables drive it. We propose PermuCATE, an algorithm based on the Conditional Permutation Importance (CPI) method, for statistically rigorous global variable importance assessment in the estimation of the Conditional Average Treatment Effect (CATE). Theoretical analysis of the finite sample regime and empirical studies show that PermuCATE has lower variance than the Leave-One-Covariate-Out (LOCO) method and provides a reliable measure of variable importance. This property increases statistical power, which is crucial for causal inference applications with finite sample sizes. We empirically demonstrate the benefits of PermuCATE in simulated and real datasets, including complex settings with high-dimensional, correlated variables.

Algorithm selection aims to identify the optimal performing algorithm before execution. Existing techniques typically focus on the observed correlations between algorithm performance and meta-features. However, little research has explored the underlying mechanisms of algorithm selection, specifically what characteristics an algorithm must possess to effectively tackle problems with certain feature values. This gap not only limits the explainability but also makes existing models vulnerable to data bias and distribution shift. This paper introduces directed acyclic graph (DAG) to describe this mechanism, proposing a novel modeling paradigm that aligns more closely with the fundamental logic of algorithm selection. By leveraging DAG to characterize the algorithm feature distribution conditioned on problem features, our approach enhances robustness against marginal distribution changes and allows for finer-grained predictions through the reconstruction of optimal algorithm features, with the final decision relying on differences between reconstructed and rejected algorithm features. Furthermore, we demonstrate that, the learned DAG and the proposed counterfactual calculations offer our approach with both model-level and instance-level explainability.

Deep models are increasingly used to analyze brain graphs for the diagnosis and understanding of brain diseases. However, due to the multi-site data aggregation and individual differences, brain graph datasets exhibit widespread distribution shifts, which impair the model’s generalization ability to the test set, thereby limiting the performance of existing methods. To address these issues, we propose a Causally Invariance-aware Augmentation for brain Graph Contrastive Learning, called CIA-GCL. This method first generates a brain graph by extracting node features based on the topological structure. Then, a learnable brain invariant subgraph is identified based on a causal decoupling approach to capture the maximum label-related invariant information with invariant learning. Around this invariant subgraph, we design a novel invariance-aware augmentation strategy to generate meaningful augmented samples for graph contrast learning. Finally, the extracted invariant subgraph is utilized for brain disease classification, effectively mitigating distribution shifts while also identifying critical local graph structures, enhancing the model’s interpretability. Experiments on three real-world brain disease datasets demonstrate that our method achieves state-of-the-art performance, effectively generalizes to multi-site brain datasets, and provides certain interpretability.

Telling apart the cause and effect between two random variables with purely observational data is a challenging problem that finds applications in various scientific disciplines. A key principle utilized in this task is the algorithmic Markov condition, which postulates that the joint distribution, when factorized according to the causal direction, yields a more succinct codelength compared to the anti-causal direction. Previous approaches approximate these codelengths by relying on simple functions or Gaussian processes (GPs) with easily evaluable complexity, compromising between model fitness and computational complexity. To overcome these limitations, we propose leveraging the variational Bayesian learning of neural networks as an interpretation of the codelengths. Consequently, we can enhance the model fitness while promoting the succinctness of the codelengths, while avoiding the significant computational complexity of the GP-based approaches. Extensive experiments on both synthetic and real-world benchmarks in cause-effect identification demonstrate the effectiveness of our proposed method, surpassing the overall performance of related complexity-based and structural causal model regression-based approaches.

For text-based AI systems to interact in the real world, causal reasoning is an essential skill. Since interventional data is costly to generate, we study to what extent an agent can learn causal reasoning from passive data. Specifically, we consider an axiomatic training setup where an agent learns from multiple demonstrations of a causal axiom (or rule), rather than incorporating the axiom as an inductive bias or inferring it from data values. A key question is whether the agent would learn to generalize from the axiom demonstrations to new scenarios. For example, if a transformer model is trained on demonstrations of the causal transitivity axiom over small graphs, would it generalize to applying the transitivity axiom over large graphs? Our results, based on a novel axiomatic training scheme, indicate that such generalization is possible. We consider the task of inferring whether a variable causes another variable, given a causal graph structure. We find that a 67 million parameter transformer model, when trained on linear causal chains (along with some noisy variations) can generalize well to new kinds of graphs, including longer causal chains, causal chains with reversed order, and graphs with branching; even when it is not explicitly trained for such settings. Our model performs at par (or even better) than many larger language models such as GPT-4, Gemini Pro, and Phi-3. Overall, our axiomatic training framework provides a new paradigm of learning causal reasoning from passive data that can be used to learn arbitrary axioms, as long as sufficient demonstrations can be generated.