Causal Identifiability

Momentum

11 papers in the last four weeks, up 83% on the four weeks before. 0.1% of all new papers.

Jul 13Week of Sep 28

Latest papers 86

Jul 13, 2026cs.LG

Relaxing Faithfulness with Intervention-Only Causal Discovery

Causal discovery algorithms learn a network that describes the causal dependencies among random variables. A common workflow involves first utilizing conditional independence properties on observational data to determine partially directed causal relationships, then applying interventions to orient the unknown causal directions. A critical assumption for the first step is faithfulness: a requirement that causally linked variables exhibit statistical dependence. Many natural systems include buffering and stabilizing pathways that cancel out to achieve systemic robustness. This cancellation of pathways violates faithfulness, leading causal discovery algorithms to incorrectly remove causal dependencies. In this paper, we argue that hard interventions contain information about the presence/absence of causal linkage that is overlooked in the first stage of structure discovery. We show that a mild assumption -- called intervention-immediacy faithfulness -- that allows cancellations, is sufficient to nonparametrically identify causal structures with hard interventions. These results position interventions as the primary carriers of information about causal structure, which should take precedence over conditional independence testing. To flip the paradigm, we also specify equivalence classes when the identification criteria are not met due to limitations in the scope of interventions.
Jul 9, 2026cs.LG

Structure Learning on Clustered Data

Recent algorithmic advances have made directed acyclic graph (DAG) structure learning scalable for causal discovery. Yet, the currently available techniques assume a completely homogeneous population, precluding their application to clustered data where cluster-specific variations (e.g., patient-specific effects) are common. We address this issue by introducing a new approach that estimates a global structure while accounting for local cluster-level effects. The key idea is to extend the fixed- and random-effects framework of classical mixed models to the structure learning setting. Towards this end, we present a differentiable graph coupling mechanism that guarantees the union of the fixed- and random-effects graphs remains acyclic. Computationally, we provide a provably convergent first-order method and leverage efficient batched updates across clusters. Statistically, we establish identifiability of the model and show that our approach recovers the true structure asymptotically. In experiments on real and synthetic data, our proposal detects dependencies missed by alternative estimators, underscoring its value for structure learning in clustered settings.
Jul 6, 2026stat.ML

Geometric Causal Models

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.
Jul 5, 2026cs.LG

Knowledge-Informed Local Causal Discovery of Optimal Adjustment Sets

Local causal discovery is a scalable alternative to global structure learning. However, it can struggle to identify valid adjustment sets in data-scarce settings because of finite-sample uncertainty, incomplete local neighborhoods, and unresolved Markov equivalence. Although many application domains provide structured background knowledge, its integration into local causal discovery remains limited. We propose b-LOAD, a knowledge-informed extension of the LOAD algorithm for local discovery of optimal adjustment sets. b-LOAD incorporates prior edge constraints directly into the local structure-learning procedure and uses Meek's rules to expand the discovery frontier dynamically, yielding a knowledge-constrained partially directed graph over the relevant local subgraph. This strategy helps prevent structurally relevant nodes introduced by prior knowledge from being excluded by local search. We prove that, under sound background knowledge, the procedure monotonically refines the admissible equivalence class and can enlarge the set of identifiable causal queries, enabling recovery of optimal adjustment sets that are not identifiable from observational conditional-independence information alone. Empirically, b-LOAD improves downstream causal effect estimation relative to purely data-driven and standard knowledge-augmented baselines, particularly in data-scarce and structurally complex regimes. Results on real-world biological networks show that locally targeted prior knowledge provides the largest gains and remains beneficial under moderate structural noise. These findings position b-LOAD as a scalable approach for converting fragmented domain knowledge into more reliable causal-effect estimation.
Jun 30, 2026stat.ME

Hierarchical Clustering As a Novel Solution to the Notorious Multicollinearity Problem in Observational Causal Inference

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.
Jun 29, 2026stat.ML

Non-parametric recovery of causal diffusion mechanisms from steady-state observations

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.
Jun 26, 2026cs.LG

Disentangling Continuous-Time Latent Dynamics: Identifiability of Latent SDEs via Diffusion Shifts

Causal representation learning for time series has developed strong identifiability results in discrete-time latent causal models, but identifiability in continuous-time latent stochastic differential equation (SDE) models remains largely open. We address this gap using environment-induced shifts in diffusion covariance. We study additive-noise latent SDEs observed through an unknown nonlinear diffeomorphism, with shared drift but environment-specific diffusion covariance. We show that two diagonal diffusion regimes with pairwise distinct coordinate-wise variance ratios identify the latent coordinates up to permutation, coordinate-wise scaling, and a possible constant shift, without any sparsity assumption on the drift. We first prove this result for linear Ornstein-Uhlenbeck systems and then extend it to general additive-noise latent SDEs. Under mild smoothness, the instantaneous drift-Jacobian causal graph is identifiable up to the same permutation. We propose a two-stage estimator for latent disentanglement and optional graph recovery; experiments on synthetic systems confirm the predicted identifiability boundary, and an application to Hardanger Bridge monitoring data illustrates the approach on real sensor trajectories.
Jun 20, 2026cs.LG

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.
Jun 18, 2026cs.LG

Temporal Causal Prior-Data Fitted Networks for Panel Data with Learned Reliability Signals

Estimating causal effects in industrial time series requires handling temporal dynamics, time-varying treatments, and unobserved confounders. Existing causal foundation models (CausalPFN, CausalFM) operate only on static cross-sectional data; neural temporal methods (CRN, G-Net) require per-dataset training; and concurrent temporal-PFN proposals have not been demonstrated at industrial scale. None output explicit per-pair reliability signals alongside their CATE estimates. We introduce Temporal Causal Prior-Data Fitted Networks (TCPFN), a foundation model for zero-shot temporal causal discovery with learned reliability signals. TCPFN makes four contributions: (1) a Causal Judgment Head that jointly predicts null-effect probability, confounding strength, identifiability, mediation fraction, and causal regime; (2) a mixed training prior covering six causal regimes (independent, direct, confounded, mediated, time-varying confounded, feedback) plus CausalFM-style front-door and instrumental-variable priors; (3) a discrete-token panel-data architecture with cross-attention masking that prevents inter-horizon leakage; (4) zero-shot inference at industrial scale via FAISS-based context selection and one-step posterior correction. On 19 benchmark datasets across five domains, TCPFN achieves competitive zero-shot causal discovery: AUROC 0.96 on Tennessee Eastman, 0.93 on SWaT, 0.98 on Causal Rivers, 0.97 on CAUSRCA. The null detector reaches NullF1 0.94, AUROC 0.99. TCPFN scales to V=1,275 on a proprietary Kraft pulp-and-paper dataset in 6 hours on a single GPU; PCMCI, a CPU-only library, on a V=666 sub-panel of the same data took 81.5 hours, extrapolating by O(V^2) to ~12.5 days at V=1,275. TCPFN's top edges identify cross-subsystem causal relationships while PCMCI's surface within-instrument controller-measurement coupling -- a scalability case study.
Jun 17, 2026cs.LG

Unsupervised Causal Abstractions Discovery

Causal abstractions formalize when a high-level structural causal model (SCM) captures the interventional behavior of a lower-level SCM. Existing applications of this notion largely follow a hypothesis-testing paradigm: an expert proposes a candidate high-level model and then evaluates if the low-level system implements it. We study the complementary problem of learning a high-level model directly from low-level measurements. Our contributions leverage hypotheses from low-rank causal discovery, and can be summarized as follows: (1) we show that observations generated by a low-rank graph induce latents that form a causal abstraction, (2) we provide identifiability results about these latents, and (3) we propose a practical objective to learn this high-level SCM.
Jun 12, 2026econ.EM

Identification and Inference for Algorithmic Frontiers with Selective Labels

This paper provides identification results to characterize a fairness-accuracy (FA) frontier, and statistical inference tools to test hypotheses and build a confidence set for the FA-frontier, when outcomes are observed only for selected individuals. When the selection process is unrestricted but loss is measured in specific ways, we provide a characterization of the sharp identification region of the FA-frontier. Under an assumption of unconfoundedness conditional on observables (and unrestricted loss functions), we obtain point identification and propose a debiased machine learning estimator, derive its asymptotic distribution, and show how this can be used to carry out inference for the FA-frontier. In work in progress, we extend the partial identification results to a broader class of loss functions.
Jun 12, 2026cs.AI

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.
Jun 9, 2026cs.AI

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.
Jun 8, 2026cs.LG

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.
Jun 6, 2026stat.ML

Beyond Additivity: Causal Discovery in Location-Scale Noise Models with Hidden Variables

We study causal discovery from observational data when some variables are hidden and the data-generating process follows a location-scale noise model (LSNM). Existing methods that handle hidden confounders typically assume additive noise, but in practice, causes often modulate not just the mean but also the variance of their effects. We prove that acyclic directed mixed graphs (ADMGs) satisfying a bow-free condition are identifiable under LSNM with hidden variables, establishing the first identifiability result for causally insufficient models beyond noise additivity. We further provide sufficient conditions for identifying causal direction even when the bow-free assumption is violated. Our two-stage algorithm, LSNM-UV, is sound and complete, and experiments demonstrate improved performance over additive baselines on heteroscedastic data.
Jun 4, 2026cs.LG

Causal Modeling of Selection in Evolution

Understanding potential selection in data is crucial for causal discovery; we argue that "selection" in common narratives takes two forms, which we term static and evolutionary selection, respectively. Static selection refers to a one-shot filtering process where observed data consist of a subset of the population of interest, as in survey volunteer bias. Evolutionary selection, in contrast, operates through repeated rounds of differential fitness in reproduction, where observed data constitute the latest generation shaped by a historical trajectory, as in immune adaptation, antibiotic resistance, and social norm emergence. Existing methods largely conflate these two forms and rely on an identical graphical model of selection. We show that this model is valid for static settings but fails to characterize data under evolution, yielding false discovery results. To address this, we introduce a new model that specifically characterizes evolutionary selection, and develop a sound and complete procedure for identifying such models from data across one or multiple environments or generations. Experimental results validate the method's ability to uncover the relevant mechanisms underlying evolution from data.
Jun 2, 2026cs.AI

Unveiling the Structure of Do-Calculus Reasoning via Derivation Graphs

The do-calculus defines a general system of inference for interventional queries, allowing causal quantities to be transformed through successive applications of its rules. This process induces a rich space of equivalent interventional expressions, but combining and ordering these rules remains challenging. In this work, we introduce derivation graphs, which represent how do-calculus rules are applied and combined, and characterize the full space of observational and interventional probabilities which are equivalent under the do-calculus. The structure of these graphs yields a simple procedure that uses at most four applications of do-calculus rules. Finally, we show how applying identification algorithms to equivalent causal queries produces multiple valid estimands for the same causal quantity, eventually yielding more efficient estimators.
Jun 1, 2026stat.ML

Identifiable Markov Switching Models with Instantaneous Effects and Exponential Families

Temporal systems often exhibit non-stationary behaviour, such as seasonal climate variation or glucose fluctuations in patients with type-1 diabetes. One way to model non-stationarity is through discrete latent regimes, i.e., stationary segments of time. Such systems induce a Markov Switching Model (MSM), a class of Hidden Markov Models with autoregressive dependencies among latent regimes and observed variables. Identifying latent regimes is challenging in the presence of frequent regime switches and nonlinear and non-Gaussian dynamics, particularly when there are instantaneous effects between the variables, e.g., due to slow rates of measurements. In this work, we establish the identifiability of both latent regimes and regime-dependent causal structures under temporal regime dependencies, nonlinear lagged and instantaneous effects, and independent noise from the exponential family. Our identifiability theory subsumes non-temporal mixtures of causal models. Furthermore, we introduce FlowMSM, a regime detection framework that can be paired with any stationary causal discovery method to recover regime-dependent causal structures. Experiments on synthetic benchmarks and a financial economics dataset demonstrate the effectiveness of our approach to detect latent regimes and discover causal structures from non-stationary time series.
May 31, 2026stat.ME

Topological Ignorability for Structural Causal Effects Beyond Means

Many interventions alter the structure of an outcome distribution rather than its mean: they can split a population into disconnected regimes, create loops or holes, generate branches, or reorganize an outcome cloud while leaving the average response nearly unchanged. In such settings, mean-based causal estimands such as the average treatment effect may miss important structural effects. We introduce topological-geometrical causal metrics based on summaries of interventional outcome laws, including density-superlevel Betti summaries, Euler signatures, and persistent-homology summaries. These metrics quantify structural differences between treated and untreated outcome laws beyond averages. We also study the assumptions needed for causal interpretation. We introduce topological ignorability, a topological analogue of conditional ignorability that requires invariance of the chosen structural feature rather than the full counterfactual distribution. When the chosen summary is injective, this condition coincides with weak ignorability; for noninjective summaries, it can identify the structural feature of interest without identifying the full interventional law. We define a covariate-standardized topological-geometrical causal effect and develop practical estimators. We validate the framework in two hidden-confounding benchmarks: a fully synthetic exact benchmark and a real-covariate semi-synthetic benchmark using Wisconsin breast-cancer covariates. In both, weak ignorability fails and balancing observed covariates nearly eliminates standardized mean differences, yet the coordinate-mean average treatment effect remains biased. By contrast, selected finite density-superlevel Betti and Euler contrasts remain stable across oracle, observational, and weighted analyses.
May 30, 2026stat.ML

Position: Prioritize Identifying Structure, Not Complex Models, for Scientific Discovery

Modern Machine Learning (ML) and Artificial Intelligence (AI) models, especially large language models (LLMs), are increasingly used to generate scientific hypotheses and mechanistic explanations from observational data. This position paper argues that in the high-dimensional proxy regimes where modern ML excels, mechanistic learning is generically underdetermined: many incompatible mechanisms induce essentially the same observational relationships on the support of the data, so predictive success and coherent explanations are insufficient evidence of mechanism discovery. This underdetermination becomes uniquely hazardous with large language models (LLMs), which tend to collapse large equivalence classes of explanations into a single fluent narrative. This paper proposes concrete standards for ``mechanistic ML,'' and argues these norms are necessary if LLM-centered workflows are to support science rather than merely simulate it.
May 30, 2026cs.LG

On the Recoverability of Causal Relations from Bulk Gene Expression Data

Bulk gene expression profiling, which aggregates pooled RNA across cells within a biological sample, remains important in the single-cell era because it is typically less noisy, more sensitive, and more cost-effective than single-cell assays. Accordingly, a growing body of computational methods seeks to recover causal relations among genes from bulk expression data. However, aggregation is a lossy, non-invertible coarsening of the underlying cellular system, and it remains unclear whether and under what conditions causal relations are recoverable from aggregated bulk gene expression data. To answer this, we formalize recoverability under aggregation through two notions of consistency: functional-form consistency and conditional-independence consistency. We then derive necessary and sufficient conditions for recoverability, showing that these properties are preserved only under linear aggregations (e.g., sum/mean) coupled with affine structural equations. To assess the practical plausibility of these conditions, analyses of four bulk and four single-cell gene expression datasets further reveal that the estimated pairwise regulatory functions among genes deviate from linearity in both data types, providing limited empirical support for the linearity assumptions required for recoverability. Together, these results caution against recovering causal relations from aggregated bulk expression data without strong additional assumptions.
May 26, 2026cs.AI

Why LLMs Fail at Causal Discovery and How Interventional Agents Escape

Causal discovery is a cornerstone of scientific reasoning, yet whether large language models can perform it reliably remains an open question. Recent benchmarks show that even fine-tuned models plateau on simple causal graphs and degrade as complexity grows, but why they fail has not been established. We prove the failure is fundamental: supervised fine-tuning, direct preference optimization, and in-context learning all produce predictors that cannot distinguish between causal graphs generating similar observational data, and any attempt to do so requires the model's internal representations to grow unboundedly, violating the very conditions under which these methods work. We formalize this as a kernel obstruction theorem, establishing that the limitation is intrinsic to the learning paradigm, \emph{not any particular model or dataset}. We propose Agentic Causal Bayesian Optimization (A-CBO), wherein a frozen language model serves as an interventional oracle answering targeted queries about intervention effects, while an external Bayesian loop concentrates beliefs over candidate graphs in logarithmically many rounds. Because the decision operates outside the space where the obstruction applies, A-CBO provably converges while the underlying model remains unchanged. On Corr2Cause, A-CBO matches fine-tuned baselines without any training. On Extended Corr2Cause, a new benchmark scaling to 24 variables with 18K test samples, A-CBO significantly outperforms both fine-tuning and preference optimization, with the advantage growing
May 26, 2026stat.ML

Iterative Causal Discovery: Per-Edge Impossibility Certificates, Tier-Aware Oracle Queries, and the 1+K1+K Lower Bound

Causal-discovery algorithms return a directed graph, yet provide no principled means of distinguishing edge directions identified by the data from those assigned without an identifying assumption. Under the standard Markov and faithfulness conditions, the observational distribution identifies only a Markov equivalence class; orientations within that class are not determined by the joint distribution and cannot be recovered from additional samples alone, but require either a functional restriction or an intervention. We introduce a protocol for observational causal discovery on continuous data that attaches to each candidate edge a discrete impossibility certificate: a RESOLVED code records the identifiability theorem under which the direction was committed, while an IMPOSSIBLE code records the failure mode together with the specific question a domain expert must answer to resolve it. The bivariate cascade is extended with five gated identifiability tiers LSNM, IGCI, Stein, MDL, and PEIT that abstain when their precondition test rejects. Two oracle primitives, the meta-hub query and the node-children query, jointly establish an upper bound of 1+K1+K expert interactions sufficient to recover any DAG, where KK denotes the number of non-leaf vertices. Under an ideal-oracle assumption, the bound is met exactly on the asia, sachs, child, and alarm benchmarks.
May 25, 2026cs.LG

Learning Latent Dynamical Causal Processes for Single-Cell Perturbation Prediction

Single-cell perturbation prediction aims to infer how cells respond to unseen interventions and to achieve out-of-distribution (OOD) generalization, providing a computational route to understanding how perturbations reshape cellular programs over time. Existing machine learning methods have made important progress, but typically capture only one side of the response. Latent causal approaches seek mechanisms that support generalization and interpretation, yet often treat perturbation effects as static outcomes. Temporal models describe how gene expression changes across time, but usually do not explicitly recover the latent causal generative mechanisms driving these changes. In practice, perturbation effects are both latent and dynamical: interventions act through unobserved cellular programs, whose states evolve over time and give rise to observed expression profiles. Motivated by this view, we propose a latent dynamical causal generative model for single-cell perturbation data that jointly captures latent cellular programs, perturbation-conditioned mechanisms, and temporal evolution. We further provide an identifiability analysis showing that, under suitable conditions, the latent causal variables are recoverable up to standard equivalence classes. Guided by this analysis, we develop CITE-VAE, a learning framework for recovering latent cellular programs and their perturbation-driven dynamics from single-cell sequencing data. Experiments on Causal-3DIdent validate the theoretical results and the effectiveness of the proposed method in controlled settings. Additional experiments on real-world CRISPR-based single-cell perturbation data show improved generalization to unseen perturbations compared with state-of-the-art baselines, highlighting the practical robustness of our approach.
May 21, 2026cs.LG

Learning Causal Orderings for In-Context Tabular Prediction

In-context learning for tabular data sets strong predictive standards in observational settings; it however primarily relies on correlational structure, which becomes unreliable under distribution shift or intervention. While established methods to discover causal structure exist, they are often focused on structure identifiability and decoupled from the predictive architectures that could benefit from them. To bridge these perspectives, we study how to simultaneously infer and enforce causal structure in the form of topological variable orderings into tabular prediction. Unlike standard architectures, our model TabOrder uses causal order-constrained attention, basing predictions only on features that precede a target under a learned causal order. Similar to causal discovery methods, TabOrder learns the optimal variable ordering in an unsupervised manner through a likelihood-based objective. We justify this choice under standard functional model classes and also study how sample missingness, a common challenge in tabular data, interacts with causal direction identification. Empirically, we confirm that TabOrder recovers accurate variable orderings while addressing prediction and imputation tasks, as well as gives insight into real-world biological data under intervention.
May 21, 2026stat.ME

Causal Discovery in Structural VAR Models Under Equal Noise Variance

Causal discovery from multivariate time series is challenging when causal effects may occur both across time and within the same sampling interval. This issue is especially important in applications such as neuroscience, where the sampling rate may be coarse relative to the underlying dynamics and contemporaneous effects need not form an acyclic graph. We study causal discovery in linear Gaussian structural VAR models under an equal noise variance assumption, meaning that the structural noise terms have a common variance. Unlike the DAG-based cross-sectional equal noise variance setting, the time-series setting considered here does not generally yield point identification of a unique causal graph. Instead, multiple structural VAR parameterizations can induce the same stationary observed process law. We introduce a notion of observational equivalence tailored to this setting and show that the corresponding equivalence class is characterized by orthogonal transformations of the structural equations together with a global positive scale. This characterization leads to an equivalence-aware model discrepancy, the observational alignment discrepancy, which compares structural models modulo transformations that preserve the observed law. Building on this theory, we propose ENVAR, a sparsity-based procedure that searches over the induced observational equivalence class for a sparse normalized structural representative. We evaluate the proposed methodology on synthetic structural VAR data and on an fMRI dataset.
May 20, 2026stat.ML

Local Covariate Selection for Average Causal Effect Estimation without Pretreatment and Causal Sufficiency Assumptions

We study the problem of selecting covariates for unbiased estimation of the total causal effect.Existing approaches typically rely on global causal structure learning over all variables, or on strong assumptions such as causal sufficiency - where observed variables share no latent confounders - or the pretreatment assumption, which limits covariates to those unaffected by the treatment or outcome. These requirements are often unrealistic in practice, and global learning becomes computationally prohibitive in high-dimensional settings.To address these challenges, we propose a novel local learning method for covariate selection in nonparametric causal effect estimation that avoids both the pretreatment and causal sufficiency assumptions. We first characterize a local boundary that contains at least one valid adjustment set whenever one exists for identifying the causal effect, and then develop local identification procedures to efficiently search within this boundary.We prove that the proposed method is sound and complete. Experiments on multiple synthetic datasets and two real-world datasets show that our approach achieves accurate causal effect estimation while substantially improving computational efficiency.
May 19, 2026cs.LG

Score-Based Causal Discovery of Latent Variable Causal Models

Identifying latent variables and the causal structure involving them is essential across various scientific fields. While many existing works fall under the category of constraint-based methods (with e.g. conditional independence or rank deficiency tests), they may face empirical challenges such as testing-order dependency, error propagation, and choosing an appropriate significance level. These issues can potentially be mitigated by properly designed score-based methods, such as Greedy Equivalence Search (GES) (Chickering, 2002) in the specific setting without latent variables. Yet, formulating score-based methods with latent variables is highly challenging. In this work, we develop score-based methods that are capable of identifying causal structures containing causally-related latent variables with identifiability guarantees. Specifically, we show that a properly formulated scoring function can achieve score equivalence and consistency for structure learning of latent variable causal models. We further provide a characterization of the degrees of freedom for the marginal over the observed variables under multiple structural assumptions considered in the literature, and accordingly develop both exact and continuous score-based methods. This offers a unified view of several existing constraint-based methods with different structural assumptions. Experimental results validate the effectiveness of the proposed methods.
May 18, 2026cs.LG

Identifiable Multimodal Causal Representation Learning under Partial Latent Sharing

Causal representation learning (CRL) seeks to uncover meaningful latent variables and their corresponding causal structure from high-dimensional observational data. Although its significance, CRL identifiability remains a crucial property, as it ensures the recovery of the mechanisms behind the data generation process, and hence the interpretability and robustness of the representation. Proving identifiability in CRL is intrinsically difficult, and we address in this work an even more challenging setting: multimodality. We consider multimodal observed data with a latent partially shared structure. Each modality is generated, through non linear mixing functions, from a specific subset of causal latent variables. Under flexible assumptions and without imposing any parametric distribution on the latent variables, we establish component-wise identifiability guarantees for the causal latent representation. Our identifiability results, furthermore, apply to the undercomplete scenario where we have, for each modality, more observed than latent variables. To instantiate our theoretical analysis, we introduce a Wasserstein-based module to recover the partially shared latent structure. Due to its differentiability, the latter can be easily integrated into all types of architecture, only requiring minimal changes. Extensive experiments on synthetic and realistic datasets validate the superiority of our approach over SOTA methods.
May 13, 2026stat.ML

Causal Learning with the Invariance Principle

Causal discovery, the problem of inferring the direction of causality, is generally ill-posed. We use the language of structural causal models (SCM) to show that assuming that the causal relations are acyclic and invariant across multiple environments (e.g., the way minimum wage affects employment rate is stable across different geographical regions), \textit{only} two auxiliary environments are sufficient to infer the causal graph for arbitrary nonlinear mechanisms. Moreover, we demonstrate that this implies identifiability of the SCM functional mechanisms: as a corollary, we show that \textit{two} auxiliary environments are sufficient to guarantee correct counterfactual inference. We empirically support our theoretical results on synthetic data.