Causal Structure Learning

Graphical approaches to causal abstraction transform a low-level causal directed acyclic graph (DAG) over many measured variables into a smaller, high-level DAG whose nodes cluster the original variables and whose edges summarize the causal relations between clusters. Such cluster DAGs are easier to interpret, but learning them requires finding the clusters and recovering the edges between them. Madaleno et al. (2026) learn the interventional coarsening (the cluster DAG that merges variables the interventions cannot distinguish) in two constraint-based phases: first the clusters, then the edges. We introduce COARSE, the first score-based method for this task: it keeps the two-phase structure but, under linear Gaussian assumptions, swaps the constraint-based edge phase for a score-based one. We show that the interventions themselves identify a causal order over the clusters, and learning the edges reduces to a single local search per cluster under a cluster-level BIC score. We prove that the procedure runs in polynomial time and, provided the variables affected by each intervention are correctly identified, that it is consistent. On synthetic and real-world interventional data, COARSE matches state-of-the-art edge recovery given enough samples, with an edge phase up to two orders of magnitude faster, including on dense graphs with hundreds of nodes.

Transformers can execute algorithms on data given in their input. We ask whether they can do the same for causal discovery. We study a standard continuous method that repeatedly updates a candidate causal graph while enforcing acyclicity. We explicitly construct a fixed-weight transformer whose forward pass exactly reproduces one update of this method, so repeated blocks reproduce its optimization trajectory. The transformer carries the current graph and the algorithm's multiplier between updates. We show that retaining the multiplier is essential for exact execution, since different multiplier values can lead to different next updates. We also give conditions under which, within a fixed stage, the number of updates needed to reach a target accuracy can be computed in advance and rounding errors stay bounded as depth grows. Experiments show that the constructed block agrees with a reference update to floating-point precision, while arithmetic replay on synthetic data and seven published benchmark network topologies inherits the reference solver's successes and failures. This separates accurate algorithm execution from accurate causal recovery. In contrast, the ordinary attention models tested under our training budgets do not reliably execute the update or transfer to larger graphs. Whether gradient training can learn an executor in the architecture class of the construction remains open.

Causal discovery becomes particularly challenging when the available sample size is small relative to the number of variables. This challenge also arises in the linear non-Gaussian acyclic model (LiNGAM), an identifiable framework for causal discovery from observational data. DirectLiNGAM estimates a causal order, which arranges variables so that causes precede their effects, by sequentially identifying an exogenous variable and removing its linear effect from the remaining variables. We establish a structural limitation of this procedure: when the number of variables exceeds the sample size, repeated residualization necessarily becomes degenerate before the full causal order can be determined. Our analysis further reveals that each residual can be reconstructed using only a graph-determined subset of variables already placed earlier in the causal order, termed the active boundary. This result motivates AdaPS-LiNGAM (Adaptive Predecessor Selection LiNGAM), which reconstructs each residual directly from the original observations using an adaptively chosen sparse subset of those earlier variables. The same subset-selection principle is also applied to the final pruning step for edge estimation. Experiments on synthetic data demonstrate that AdaPS-LiNGAM provides accurate causal-structure recovery in sample-limited settings and degrades more gradually as the sample size decreases.

Learning a directed acyclic graph (DAG) from observational data is a challenging combinatorial problem due to the exponential growth in the number of candidate parent-set configurations. Existing exact score-based methods often require computationally intensive combinatorial search, whereas constraint-based methods can become unreliable or computationally demanding as graph size and conditioning-set complexity increase. We develop a non-parametric hybrid framework, referred to as DECO (Directional Evidence-guided Configuration Optimization), that extracts dependency and directional evidence from observation data to construct admissible parent sets prior to exact optimization. It reduces the optimization search space by eliminating empirically unsupported parent configurations while preserving flexibility for all plausible edge orientations. Theoretical analysis establishes an exponential reduction in the admissible parent-set configuration space and quantifies how bounded edge-level omission affects the probability of retaining the true parent structure. Experiments on benchmark Bayesian networks and synthetic discrete and continuous DAGs demonstrate substantial search-space reduction while achieving competitive structure-recovery performance, with favorable structural Hamming distance across many evaluated settings. These results show that directional evidence can provide an effective preprocessing mechanism for reducing the computational burden of exact DAG learning without requiring a fixed parametric structural~model.

Discovery of causal relationships in high-dimensional Gene Regulatory Networks (GRN) is computationally challenging and often difficult to interpret due to dense connections. Therefore, grouping genes together into functional modules can improve tractability and biological interpretability. However, existing cluster level causal discovery methods assume access to a predefined admissible partitions, requiring the graph over clusters to be acyclic. Constructing such partitions is therefore challenging. In this work, we introduce GO-based Clustering for Causal Discovery (GO4CD), an algorithm that uses Gene Ontology (GO) to construct biologically meaningful gene partitions at multiple levels of granularity, while favoring those more likely to be admissible for causal discovery. GO4CD groups together genes participating in a shared biological process, and propagates gene annotations through the ontology hierarchy to achieve different granularity of partitions. Furthermore, we integrate GO4CD with Causal Learning over Clusters (CLOC) algorithm and evaluate recovery of true Markov equivalence class both with an oracle of conditional independencies and on simulated gene expression data using multivariate conditional independence tests. We evaluate GO4CD on multiple E.coli regulatory subnetworks and find that it is inadmissible in 18.1% of the cases, compared with 65.3-82.3% for the semantic-similarity baselines. Our results indicate that GO4CD is substantially better suited to learning causal GRNs defined over biologically meaningful gene clusters.

Causal representation learning aims to discover robust features by exploiting the causal structure underlying data generation. Existing methods require specifying the causal structure a priori, yet different structures demand fundamentally incompatible invariance constraints, and misspecification leads to representations that discard predictive information. We introduce SaCRL, a framework that jointly identifies the causal structure and learns the corresponding invariant representation without prior structural knowledge. Our approach formulates structure selection as a soft optimization over candidate invariances using HSIC-based violation metrics, with adaptive weights that automatically concentrate on the achievable structure. We provide theoretical guarantees for structure identification, including under random-feature approximation, invariance satisfaction, and out-of-distribution generalization. Empirically, SaCRL recovers the true structure on synthetic and semi-synthetic Bayesian-network benchmarks, outperforms fixed-invariance baselines on Colored MNIST, achieves state-of-the-art accuracy on three DomainBed benchmarks (PACS, VLCS, OfficeHome), and degrades gracefully under structural misspecification and limited environment diversity. Code is available at: https://github.com/ArmanBehnam/sacrl.

We study causal structure learning from observational data in linear Gaussian structural causal models in the presence of directed cycles and an unknown number of exogenous latent confounders, bounded by a given maximum. We derive the covariance of the observed variables and introduce marginal quasi-equivalence, which characterizes when different causal models share a full-dimensional subset of the observational distributions they can generate. We formulate structure learning as minimization of the Gaussian negative log-likelihood with a logarithmically scaled complexity penalty that counts directed edges and latent variables. For a fixed number of observed variables and a fixed upper bound on latent variables, we establish consistency of global score minimizers up to marginal quasi-equivalence under algebraic faithfulness, structural minimality, and model-overlap assumptions. We parameterize the inclusion of directed edges and candidate latent variables using Bernoulli gates, whose continuous probabilities are optimized jointly with the structural coefficients. Averaging the penalized negative log-likelihood over these gates yields an objective with a closed-form differentiable complexity penalty. We prove that this expected objective has the same global infimum as the corresponding discrete structure-learning objective. Experimental results show that our approach achieves lower recovery error than previous methods in several experimental settings.

Supervised causal discovery learns to infer causal structure for a new dataset from training datasets paired with structural labels. These training pairs are typically simulated, making the simulator both a source of supervision and a carrier of assumptions about causal graphs, mechanisms, and noise. Understanding the resulting predictions therefore requires examining how these assumptions supplement the information available in observational data, which may be compatible with multiple causal graphs. This paper examines that relationship across representative methods available through June 2026. We organize these methods by prediction target, prediction granularity, encoder, structural decoder, and training regime to relate what each method predicts to how it uses data and simulator-based supervision. Using this framework, we distinguish two questions: whether the target is identifiable under the assumed model class, and whether a trained predictor generalizes beyond its training distribution. Restrictions on mechanisms and noise can make otherwise ambiguous causal directions identifiable, but predictive accuracy under those restrictions does not establish transfer when they change. This distinction motivates evaluation that matches metrics to the identifiable graph target and tests changes in graphs, mechanisms, and noise between training and deployment. Extending such evaluation to real data also requires documenting the external causal evidence and uncertainty behind benchmark reference graphs. Together, these analyses guide method comparison and identify open questions in transfer, test-time adaptation, and uncertainty assessment.

Latent world models are trained to predict what happens next, so nothing in their objective separates what an action caused from what merely co-occurred with it. Object-masking models such as C-JEPA intervene on what the predictor can see; we intervene on what physically happens. From one saved simulator state we run the dynamics under an action $a$ and under a reference action $a_{\varnothing}$, and train the model to predict the difference $Δz=z^{a}-z^{a_{\varnothing}}$ between the two latent futures. The resulting objective, Do-JEPA, has an effect loss, a support loss (where the action enters), a propagation loss (where its effect travels) and invariance losses (what must not change). In a synthetic system with object-aligned variables, support supervision finds the directly intervened object in 99.95% of test cases, where a sparse action mask sends the action to a nuisance slot in every case, and response-onset supervision recovers the ring-shaped propagation graph (edge AUROC 0.975 vs. 0.624). From pixels, the effect loss beats a control trained on exactly the same data: it lowers latent effect error by 28.4% on an end-to-end LeWM model and physical effect error by 13.5% when trained and tested on natural action sequences, and on three independently generated CausalWorld benchmarks it lowers responsive effect error by about 20% under physics shifts and the latent context sensitivity of predicted effects by 66%. Trained from scratch it costs factual accuracy; fine-tuning an existing model with it removes this cost. Together, these results show that intervening on the world, rather than on what the model sees, helps latent world models predict what their actions cause.

A non-significant coefficient in a dynamic panel model need not imply the absence of a relationship. It may instead reflect heterogeneous effects averaged toward zero, reciprocal dynamics overlooked by a recursive specification, or relationships masked by the omission of correlated covariates. Standard linear estimators cannot distinguish among these possibilities. We develop an inferential workflow for political panel data that resolves this ambiguity by combining flexible autoregressive estimation, forecast-necessity testing, functional characterization, and same-data linear benchmarking. The workflow first identifies relationships required for out-of-sample prediction, then characterizes their functional form across political contexts, and finally, distinguishes differences arising from estimator flexibility from those due to model specification. Applied to the causal sequence model of democratization on the V-Dem panel of 113 countries, the workflow reproduces the model's central finding - the protective belt of civil society, the rule of law, and institutionalized parties - while recovering reciprocal relationships from democracy to its institutional supports that a linear model cannot detect. Most importantly, three weak published direct effects, of which two are null, and one is marginally significant, receive three different diagnoses: one dissolves under the full specification, one reflects heterogeneous effects averaged toward zero, and one was masked by the reduced variable set. The workflow corrects the published record in both directions, removing one relationship and recovering two. More broadly, the workflow provides a framework for evaluating dynamic political theories under a model class capable of representing nonlinear and reciprocal mechanisms while preserving relationship-level interpretation and explicit inferential standards.

What determines the unavoidable sample cost of learning cyclic causal structure? For cyclic linear non-Gaussian models, we study exact condensation recovery from observational data: identifying the strongly connected component (SCC) partition and all edges between components. We establish the first information-theoretic lower bounds on sample complexity for this target. For $p$ variables, maximum SCC size $s_{\max}$, and maximum external-parent count $d_B$, any estimator requires order $s_{\max}\log(ep/s_{\max})+d_B\log(ep/d_B)$ samples in the worst case over a regular model class. These bounds distinguish the costs of SCC membership and external-parent selection. Under principal invertibility and without correlation faithfulness, we establish a population block-exogeneity principle that identifies unknown root SCCs through residual independence and inclusion minimality. A sparse-adjustment characterization shows that small adjustment sets suffice to identify SCCs and their direct external parents, without regressing on all previously recovered variables. These characterizations yield BlockExo, which attains a structurally matching sample bound without knowing $s_{\max}$ or $d_B$ under suitable conditions. Simulations support the structural dependence of our sample bound and demonstrate BlockExo's sample-efficient recovery in comparisons with other methods for cyclic causal discovery.

Explanations are central to causal reasoning, and cognitive science has long established that the human drive to explain is itself a mechanism for learning about causality. Despite this, learning from those abductive signals is largely ignored in artificial intelligence. While explainable AI (XAI) increasingly draws on causal models to generate explanations, the converse direction about what explanations can do for causality remains largely unexplored. To fill this gap, we propose xWhyL, a formal framework connecting causality and XAI by learning causal models from explanations. We develop a mathematical theory that translates explanations into a learning signal complementary to observational data, and demonstrate how it enables overcoming the limits of observational causal discovery. As explanations can be derived from incorrect beliefs and clash with data, a tension we call the Causal Tug-of-War, we prove conditions under which our framework rejects misspecified explanations rather than absorbing them. Our practical instantiation, Causal Interactive Learning (CIL), shows how expert explanations can efficiently support causal discovery and distinguish correct from incorrect explanations.

Uncovering latent variables and their causal relations from observed data is a fundamental yet challenging problem. Existing methods often rely on restrictive assumptions, such as linear relations or invertible mixing functions. To better address this problem under general nonlinear mixing procedures, we propose a condition called the cross-Hessian Rank Constraint (HRC), which serves as a primitive rank-based tool for nonlinear latent causal discovery. In particular, we show that a rank-based property arises from the cross-Hessian of the observed-data log-density in the nonlinear case, revealing information about the latent variables, and reduces to the Tetrad constraints in the linear Gaussian case. More specifically, when two groups of observed variables are d-separated by a set of lower-dimensional latent variables, the rank of this cross-Hessian is equal to the dimension of the latent variables, under a mild affine derivative assumption on the conditional log-density derivatives. This assumption can be naturally satisfied when the noise level is low or the relevant nonlinearity is moderate. As a downstream application, we instantiate HRC in the pure one-factor measurement setting for locating latent variables and recovering their causal structure up to Markov equivalence. Experimental results on synthetic and real-world datasets support the theoretical claims.

Causal discovery from observational data is a fundamental yet challenging task in scientific research. While existing approaches are primarily based on conditional independence tests, structure scores, or restrictive functional assumptions, we propose Decoupled Causal Discovery (DCD), a novel decoupling-based perspective that does not rely on these methodologies. DCD directly identifies the Markov boundary (MB) by decoupling non-target variables via weighting functions, such that only variables within the MB preserve dependence with the target under the decoupled distribution. Building on this, DCD iteratively constructs the Completed Partially Directed Acyclic Graph (CPDAG) by exploiting structural asymmetries within the MBs. We establish the theoretical identifiability, soundness, and completeness of DCD. Empirical evaluations demonstrate that DCD achieves strong performance, particularly excelling in challenging noise regimes.

Large language models (LLMs) have been applied to causal discovery, but candidate-graph generation rarely treats premature omission of potentially relevant causal relations as an explicit design objective. We propose MaSCoD, a multi-agent framework that organizes candidate third variables and local structural patterns before direct-edge judgment. We evaluate MaSCoD on Auto-MPG, DWD, and Sachs using GPT-5.4 as the primary backbone and GPT-4o for replication. MaSCoD exhibits a dataset- and backbone-dependent retention-selectivity profile rather than uniform superiority. Across all six dataset-backbone settings, Full, which supplies structural hypotheses before direct-edge judgment, achieved higher mean Recall and F1 than No Phase 1, which instead constructs them within the judgment procedure, while also increasing false-positive rates. Additional reference-edge retention over all evaluated baselines was observed on DWD with GPT-5.4 and on Sachs with GPT-4o, rather than uniformly across settings. Partial ablations showed that supplying both information components did not always outperform supplying only one. For GPT-5.4, stage-wise analysis showed that the Full-No Phase 1 retention gap was already present after direct-edge judgment, while reconciliation introduced additional reference-edge loss for Full on Sachs. These findings support structural pre-organization as an explicit design and evaluation target for omission control and motivate evaluating context construction jointly with its utilization in judgment.

Causal discovery aims to recover causal relationships from observed data. In various fields, exploring causal relationships among variables remains an important topic, but this task becomes challenging due to the existence of latent confounders. Ignoring such confounders can lead to false associations and incorrect edge directions. In this paper, we study the linear structural equation model with latent confounders. We propose an algorithm that iteratively identifies terminal (observed) nodes and reconstructs the directed acyclic graph of the observed variables. To do this, we recover the precision matrix of the observed variables as a sparse plus low-rank matrix: a sparse matrix captures the conditional dependencies among observed variables, while a low-rank matrix captures the combined influence of a few latent confounders. We establish that for $p$ observed variables, $r$ latent confounders and $s$ edges, our procedure correctly identifies the directed causal relationship among observed variables, for $n \gtrsim \max\{s\log p,\ r p\}$ samples. Experimental results validate our theoretical contributions.

The problem of identifiability in linear parametric models (LPMs) whose nodes follow either an ordered logit model or a regular one-parameter exponential family is evaluated. The results go beyond classical structural equation models as well as results for nodes with observations from a homogeneous family of distributions. The main result establishes that the orientation of every edge joining an ordinal node to an exponential-family node is identifiable from the joint distribution alone at every parameter value, provided the ordinal node has at least three categories and the exponential-family node at least three points of support, with no restriction on the sufficient statistic. Converses show that both requirements are necessary: the three-category requirement is binding only for affine sufficient statistics, and the three-point requirement is binding under the canonical link. The guarantee extends to orienting every such mixed ordinal-exponential family edge of a given $d$-node undirected skeleton. Numerical experiments illustrate the theoretical results by successfully separating orientations within a Markov equivalence class, which are indistinguishable by conditional independence alone.

In networked dynamical systems, the parameter of primary mechanistic interest is signed interaction structure. Recovering this structure from perturbation time-series data is a fundamental identification problem, compounded by three coupled obstacles: the combinatorial complexity of interaction architectures, ambiguity of causal attribution under limited interventions, and state-dependent dynamics that confound structural inference. Each obstacle is structural in origin and calls for a structural solution. We address these challenges by adopting a reductionist approach, introducing Fundamental Dynamical Units (FDUs): signed three-node interaction patterns as composable primitives that convert the interaction hypothesis space into a finite, constructive, and tractable representation. We show that local interaction structure determines the perturbation conditions required to disentangle direct from relayed influence, making intervention design a structural consequence of the FDU representation. We embed FDU-regularized structural inference within a physics-informed neural ordinary differential equation (ODE) whose governing-equation constraint transforms structural hypotheses into verifiable dynamical predictions, enabling joint recovery of interaction structure and perturbation-resolved trajectories. Validated on synthetic benchmarks with known ground truth, the framework supports structural commitment, expressed through FDU primitives, motif-prescribed intervention design, and physics-informed learning, as a principled basis for mechanistically interpretable inference in networked dynamical systems.

We present a method for recovering the moral graph of a causal DAG from a probability distribution over discrete variables, using fully connected tensor networks (FCTNs) with nuclear-norm-regularized bond corrections. Each bond matrix is parameterized as a baseline all-ones matrix plus a low-rank correction $C_{ij} = U_{ij}V_{ij}^\top$, and the nuclear norm of the correction implemented via the variational Frobenius norm penalty on the factors drives unnecessary bonds to zero. We prove that under faithfulness, positivity, and a no-implicit-rerouting assumption on the local tensor architecture, \textbf{every} optimal FCTN with zero reconstruction error $\varepsilon = 0$ has effective graph exactly equal to the moral graph. For the approximate regime ($\varepsilon > 0$), we provide explicit recovery bounds using the Fannes-Audenaert continuity of conditional mutual information, and derive a sufficient condition on the regularization parameter $β$. The effective graph is read directly from the optimized bond matrices.

Smooth acyclicity constraints answer whether a weighted support is a DAG, whereas structure learning asks which support change should be made. Existing analyses establish degeneracy for particular constraint formulas but do not isolate what follows from smooth exactness itself. At a DAG boundary, we show that minimal cycle completions generate a squarefree monomial ideal containing every restricted Taylor jet of an exact representation. If the smallest completion has $q$ edges, the first possible response has order $q$ for a vector residual and $2q$ for a nonnegative scalar. Exponentially many constant-scale cyclic manifolds exhibit the same lack of ranking away from the boundary for NOTEARS and DAGMA. We derive the exact selection time for an isolated cycle. When $Ψ'(h)\asymp h^ν$, the feasibility-only time is $T_0(\varepsilon)=Θ(\varepsilon^{-(2ν+1)})$; a score margin changes the leading dynamics at scale $T_0^{-1}$ for $ν>0$, while $ν=0$ has a logarithmic boundary layer requiring $γT_0\log(1/\varepsilon)\to0$. Experiments verify this law, and a truth-free separation statistic predicts selection time on 320 official NOTEARS/DAGMA trajectories (Spearman $-0.52$ and $-0.66$, permutation $p<10^{-4}$). For finite samples, a parent-set confidence family and forced-opposite queries certify skeleton and unshielded-collider labels shared by every population optimum of a frozen score. Across 320 runs, every regret bound covers an independent oracle-score audit. None of 3,042 certified skeleton or 2,396 collider labels disagrees with the oracle-score optimum, although 4.4% and 5.5%, respectively, disagree with the generating graph. These results separate DAG feasibility, score-based support selection, and causal identification.

Probabilistic logic programming is a formalism of statistical relational artificial intelligence that supports causal queries, including interventions from outside the system. When the structure of a probabilistic logic program is learned from data, however, only probabilistic information is used, and a single probability distribution may be compatible with several causal orders. This leads to ambiguity in interventional reasoning, raising the question of when the causal order is uniquely determined by the distribution. Exploiting the relationship between acyclic probabilistic logic programs and Bayesian networks, we derive conditions under which the probabilistic information encoded in a program determines a unique causal order. We also incorporate constraints arising from relational structure by taking into account prescribed sets of causal symmetries induced by the underlying relational vocabulary. The result is a method for verifying when a learned probabilistic logic program supports well-defined intervention semantics.

Causal Discovery (CD) from observational data faces two fundamental challenges. First, purely statistical methods often lack the power to resolve structural ambiguities in low-sample regimes. Second, although LLM-assisted hybrid approaches improve structure recovery through semantic reasoning, the influence of that reasoning on individual edge decisions remains largely opaque. Consequently, existing hybrid methods fail to satisfy a fundamental requirement: explaining why a particular edge is included or excluded in the learned directed acyclic graph (DAG). This is critical in real-world applications, where no ground-truth DAG exists and every structural decision must be independently justified. We formalize this requirement as decision traceability, requiring every inferred edge to be supported by auditable statistical evidence, Markov Blanket consistency, or explicit domain reasoning. We propose GENESIS, an explainable hybrid CD framework that decomposes graph construction into interpretable decision points. GENESIS first identifies and scores three-node structural motifs, including chains, forks, and colliders, to establish transparent structural priors, then progressively refines the graph by integrating these priors with observational evidence, invoking domain knowledge only when statistical evidence is insufficient. By design, every edge decision is resolved through an auditable source of evidence. Experiments show that GENESIS achieves 100% decision traceability across all settings, establishing explainability as a first-class objective in causal discovery. Despite this additional requirement, GENESIS consistently outperforms purely statistical CD methods on the majority of benchmark datasets across all sample regimes in terms of Structural Hamming Distance (SHD), while achieving performance comparable to state-of-the-art LLM-assisted approaches.

In model-based reinforcement learning, world models exist as internal simulators, but their training often conflates statistical correlations with causal mechanisms. This problem is exacerbated in multi-agent systems where physical transitions are intertwined with strategic agent intents, causing world models to fail under distribution shift. We introduce Implicit Causal World Models to recover environmental dynamics from offline demonstrations without requiring pre-defined causal graphs. By incorporating policy variance, we render world models discoverable via the sequential backdoor condition. Evaluations across coordination tasks (Two-Door, Navigation, and Giveway) demonstrate that these models provide interpretable causal representations under both full and partial observability, with model accuracy scaling directly with interventional strength.

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.

Discovering the direct causes and effects of a target variable from observational data is a fundamental problem in causal discovery, with broad applications in domains such as gene regulatory analysis and biomedical research. Existing causal discovery methods either learn a global causal structure, which incurs substantial computational cost, or assume the absence of latent variables and selection bias, assumptions that are often violated in real-world settings. Motivated by these challenges, we study local causal structure learning in the presence of latent variables and selection bias. Specifically, we first characterize a local region that enables target-specific causal discovery without recovering the entire global structure. We then establish a theoretical bridge between causal information learned from the observed distribution induced on this local region and the corresponding information in the global causal structure. Building on these foundations, we propose LoCaLS, a local causal structure learning algorithm that is sound and complete under standard assumptions and identifies the same direct causes and effects of a target variable as those identifiable by global causal discovery methods, while allowing for latent variables and selection bias. Extensive experiments on random and real-world structures demonstrate that the proposed method consistently achieves higher structural accuracy than existing local methods while requiring substantially less computational effort than state-of-the-art global methods. Furthermore, applications to two real-world gene expression datasets reveal biologically plausible target-specific causal structures, demonstrating its practical applicability in large-scale biological data analysis.

Causal discovery methods have shown strong performance in temporal systems, but they typically rely on regular and discrete lag structures, limiting their applicability to regularly sampled data. However, many real-world tasks require dealing with irregularly sampled streams of events, such as sensor streams, healthcare data, and financial transactions. In this work, we propose an extension of PCMCI+, a state-of-the-art method for causal discovery on regular multivariate time series, to allow for handling irregular time series. Instead of modelling causal relations through fixed-lag dependencies, our method aggregates causal influence over predefined temporal windows. We evaluate our method on synthetic irregular event streams with known causal structures under different signal-to-noise ratios, showing that it consistently recovers the underlying causal graph and substantially outperforms the standard PCMCI+ on irregularly sampled data.

Expert background knowledge is often available in practical applications of causal discovery. Such constraints on the true causal graph can help causal discovery in terms of identifiability of causal effects and accuracy of the learned structure, but also in reducing the space of candidate causal graphs. As causal discovery can become computationally expensive for large number of variables, it is crucial to utilize background knowledge effectively during the causal discovery process. However, most current methods only use background knowledge in a postprocessing step after causal discovery to refine the learned graph. In this work, we develop a framework for utilizing background knowledge during the causal discovery process, focusing especially on scalable causal discovery methods that recover only a subset of the whole graph. We implement our framework for multiple algorithms and empirically show that utilizing background knowledge can both reduce computational requirements and increase the quality of the learned structures.

Causal discovery from unstructured data is a challenging yet underexplored task in high-expertise domains such as healthcare, finance, and education. Existing methods typically leverage the general knowledge of large language models (LLMs) to identify causal factors from unstructured data and annotate them into structured data for causal graph construction. However, they remain limited by two key challenges (CHs): (CH1) insufficient identification of latent factors, which are implicit in the data yet essential for causal discovery, due to the lack of domain-specific knowledge; and (CH2) unreliable factor annotation, caused by the lack of domain-grounded reasoning, which propagates errors to the resulting causal graphs. To address these challenges, we introduce a novel Domain Knowledge-enhanced Causal Discovery framework (DKCD) for causal discovery from unstructured data in high-expertise domains with three interconnected components: (1) Knowledge Mining: It retrieves relevant domain knowledge based on observable factors to support subsequent causal reasoning. (2) Knowledge-guided Causal Reasoning: Reasoning with relevant knowledge, it discovers latent causal factors to address CH1 and generates key causal clues for more accurate data annotation to address CH2. (3) Causal Structure Discovery: It constructs the final causal graphs based on a more complete factor set and accurate annotations. Experiments on two domain-specific datasets show that DKCD significantly improves both causal factor identification and causal graph construction.

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.

Algorithmic recourse addresses the challenge of providing tailored recommendations to users affected by unfavorable machine learning decisions, in potentially high-stakes scenarios. Traditional approaches to recourse often rely on the closest counterfactual explanations or assume a priori knowledge of a user's causal structure, resulting in interventions that overlook individual contexts and specific feature interactions. To overcome these limitations, we study a human-in-the-loop framework that iteratively approximates the user's structural causal model through interactive queries via Bayesian inference before producing recourse recommendations. This framework exploits humans' feedback to improve the identification of causal effects, allowing personalized recourse that is plausible, cost-effective, and aligned with the actual causal dependencies of each user. As a proof of concept, we evaluate this framework through simulated human responses. Our simulations across linear and non-linear causal models show promising results, though challenges remain in capturing complex, non-linear structures, emphasizing the importance of accurate approximations and robust noise distribution modeling.