Structural Causal Models

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.

Counterfactual inference in Gaussian-process structural causal models (GP-SCMs) has been developed primarily for continuous endogenous variables, limiting applicability to causal graphs that contain discrete child nodes with continuous parents. We introduce a unified probabilistic framework for counterfactual inference with heterogeneous variable types by pairing GP predictors with explicit exogenous noise mechanisms. For discrete outcomes, we derive exact conditional noise-abduction procedures using a uniform threshold for binary variables, a Gumbel-max race for nominal categories, and a latent Gaussian cut-point model for ordinal ones. In each case, we propagate abducted noise through interventions while accounting for posterior uncertainty in the GP latent functions, and prove that the resulting mechanisms reproduce the fitted model's observational and interventional distributions. On synthetic SCMs with known ground-truth counterfactuals, we evaluate estimation accuracy, consistency, and robustness to coupling misspecification. A key finding is that applying a categorical coupling to ordinal data inflates counterfactual error roughly threefold even when observational fit remains comparable, and that this error does not diminish with more data. As the training set grows, the fitted structural equation converges to the truth while the counterfactual error flattens onto a floor. In the reverse direction, forcing a false order onto nominal data instead degrades the fitted equation itself. The choice of coupling must therefore be justified on structural grounds rather than read off the fit.

Patient world models used for clinical trial simulation can agree on transition kernels and arm-specific risks, yet disagree on the fraction of patients harmed by switching treatment---the counterfactual quantity that matters for intervention-aware reasoning. We audit this reliability gap in a two-stage shared-response SCM: a categorical intermediate health state is followed by common terminal care. Under independent stages, the sharp harm interval has closed-form endpoints for at most three intermediate states, with an exactness boundary at four states. Declared dependence and response-mismatch budgets yield calibrated outer bounds when stage independence or complete mediation is relaxed; in a symmetric three-state model the entire sensitivity frontier is sharp, $[0,\min\{1/2,1/3+(ρ+δ)/2\}]$, and shows exactly how budgets erase the gain over endpoint-only bounds. Two eight-variable response LPs propagate interventional uncertainty for finite-sample audits. Exact witnesses verify attainability. On public clinical simulators (EpiCare; sepsis), native configurations show little resolved stage dependence and no additional joint-compatibility gain over pairwise transport---honest negative results for reliability claims. All experiments are locally reproducible; guarantees remain conditional on the stated causal model. The results provide a concrete protocol for deciding when a patient world model is safe to trust for counterfactual harm.

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.

Root cause analysis (RCA) is a critical problem in many real-world scenarios. RCA enables the identification of faulty or failing mechanisms in a system by comparing anomalous observations with corresponding reference (i.e., regular) observations. However, existing approaches rely either on heuristic methods or on conditional independence tests with a strong unconfoundedness assumption, and thus fail to exploit other complicated distributional constraints in the presence of latent variables. To relax these assumptions, we model the underlying system as a causal model and the anomalous system as a change in the structural functions of the same causal model. Specifically, to handle unobserved confounders, we establish an implicit connection between distributional constraint testing and root cause analysis. To adapt our approach to data generated from arbitrary causal models, we employ the deep causal model (DCM) framework, in which we design the causal model using neural networks. Finally, we illustrate how our method, RCA-DCM, can utilize different levels of partial graphical knowledge to perform RCA. We evaluate RCA-DCM against state-of-the-art baselines on simulated datasets, a physics-based causal chamber and two micro-service applications. RCA-DCM improves top-1 accuracy over the strongest baseline on both Sock Shop (0.880 vs. 0.752) and Online Boutique (0.776 vs. 0.712), and when the true root cause in the causal chamber is unobserved and acts as a latent confounder, it recovers the exact root-cause set more often than any competing method (perfect recovery rate (PRR) 0.846 vs. 0.731).

Structural causal models for time series recover contemporaneous and lagged effects, but most methods require complete observation windows and become misspecified when samples are missing. We introduce ITSY, the first continuous-optimization method for causal discovery from irregular time series under a linear model. ITSY reformulates the structural equation so that prediction uses the nearest available history rather than the possibly missing current slice, and jointly imputes missing values while learning both graphs. A weighted reconstruction objective corrects the noise transformation induced by this reformulation. Across synthetic regimes varying missingness, scale, graph density, and noise, and on a real world benchmark, ITSY consistently improves graph recovery over representative SCM-based baselines, demonstrating the effectiveness of the proposed method. The results establish a focused solution for irregular linear first-order dynamics and clarify the assumptions required for nonlinear or higher-order extensions.

Causal discovery from observational data is fundamental to statistics and machine learning, yet determining causal direction without interventions necessitates structural assumptions. Existing identifiability research primarily focuses on continuous variables under additive noise models, often neglecting mixed datasets containing ordinal scales, counts, and continuous measurements. This paper investigates causal discovery in Directed Acyclic Graphs (DAGs) where nodes follow either an ordinal distribution (via an ordered logit model) or a regular one-parameter exponential family distribution. We prove that the edge direction between an ordinal and an exponential family node is distributionally identifiable for generic parameter values. Our findings generalize previous Ordinal-Poisson results to the broader exponential family. Computationally, we introduce a score-based exhaustive search and a masked continuous optimization framework using DAGMA for larger graphs. Numerical results validate the theory, recovering edge orientations within a Markov equivalence class that are unidentifiable under classical structural equation models.

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.

Causal discovery aims to uncover causal structures from data and is fundamental to scientific reasoning and intervention-based decision making. Its evaluation relies heavily on structural causal models (SCMs), which specify a causal graph together with the mechanisms that generate data, yet existing studies differ substantially in graph families, mechanisms, and evaluation protocols. The emergence of causal discovery foundation models (CDFMs) further complicates evaluation: performance may reflect not only causal discovery ability, but also overlap between pretraining environments and test SCMs, making results on fixed synthetic benchmarks difficult to interpret. We introduce CausalArena, a unified and evolvable benchmark for causal discovery under a common protocol. Synthetic SCMs supply controlled breadth over structures and mechanisms; semantic operational SCMs provide human-auditable, semantically grounded environments beyond standard synthetic generators; and formula-grounded SCMs test discovery under explicit scientific mechanisms. Public real-world datasets provide an additional external-validity check. Experiments across classical, neural, and pretrained methods reveal substantial ranking shifts across SCM families and protocols, showing that strong performance in one benchmark regime does not reliably transfer to others. These results highlight benchmark diversity and pretraining--evaluation overlap as central challenges for evaluating causal discovery in the foundation model era.

Explaining why a specific outcome occurred, and which inputs deserve the blame or credit, is central to philosophical, scientific, and policy analysis. Existing tools split into two camps. The theory of actual causality (AC) gives principled verdicts, but only for toy-sized models, because computing them requires enumerating counterfactual scenarios. Scalable attribution methods like SHAP (or even causal SHAP) at least partially ignore the causal structure that generated the data, and can give answers that conflict with a careful causal analysis. We close this gap with Probabilistic Causal Impact (PCI). PCI builds on actual causality and on Pearl's notions of probability of necessity and sufficiency, but recasts the question of explainability as an estimation problem on a probabilistic causal model that is easily approximated via Monte Carlo. By specifying a distribution over "candidate explanations," a distribution over counterfactual values, and a scoring function, PCI provides tractable, causally grounded, graded explanations, generalizing AC and Pearl's probability of causation as degenerate cases. We evaluate PCI in synthetic and real-world examples, spanning consistency checks with AC, scaling experiments, complex continuous-valued dynamical systems, and a real-world deployed causal machine learning model trained on millions of datapoints.

In this paper we study linear non-Gaussian acyclic models (LiNGAM) when used in federated environments. These causal models allow one to go beyond Markov equivalence. However, in many domains data are scarce, and increasing the sample size by centralising data from different clients is not advisable due to regulations such as the GDPR. The federated environment offers an attractive option to balance privacy and causal discovery accuracy. Unfortunately, the standard centralised estimator in the LiNGAM setting, i.e., DirectLiNGAM, cannot be straightforwardly federated. Higher-order cumulant tensors offer a way around this obstacle: they depend only on the joint distribution of the variables involved and add exactly across independent sample groups, so a single communication round suffices in horizontal, vertical, and hybrid partitions. However, FedISHC, i.e., the current federated method along these lines, breaks down under near-symmetric noise. To overcome the above limitation, we introduce the FedRCD family of causal discovery algorithms, and investigate three variants that trade off communication rounds against algebraic noise; two of them are exact federated counterparts of the centralised high-order cumulant (HC) and HC-LiNGAM algorithms, and the single-round variants further effectively support exact unlearning at any granularity, from a single observation to a whole client. Numerical experiments show that at sample sizes typical of real deployments, the entire cumulant-based federated family does not actually rank variables by the population asymmetry that the scores encode at zero. It ranks them by a variance ladder induced by the DAG along its directed paths, the cumulant counterpart of varsortability. Marginal standardisation collapses every cumulant method to near-random ordering, while scale-invariant DirectLiNGAM, not federable under this protocol, is unaffected.

Scientific discovery depends on the ability to form hypotheses, test them through experiments, and revise them when evidence disagrees. Existing LLM agents support this process by improving their reasoning or actions, but their scientific beliefs are often scattered across free-form reasoning and difficult to update coherently. This makes it difficult to identify what failed, what should change, and whether revisions remain consistent with prior evidence. We introduce EvoSCM, which represents scientific beliefs as a population of structural causal model (SCM) hypotheses that can be tested and revised across experiments. EvoSCM formulates scientific discovery as a closed loop in which causal hypotheses guide experimentation and experimental outcomes drive causal model evolution. Competing SCM hypotheses make falsifiable predictions and guide discriminative experiments that separate alternative explanations. When observations contradict these predictions, EvoSCM distills discrepancies into correction rules identifying which aspects of the hypotheses fail to explain the evidence. These rules guide revisions to causal dependencies, latent factors, mechanisms, and parameters. Revised hypotheses are validated against accumulated evidence and carried forward to guide subsequent experiments, allowing scientific beliefs to evolve cumulatively. We evaluate EvoSCM across physics, chemistry and materials, and biology. It consistently outperforms baseline agents and existing evolution methods, yielding more accurate explanations and predictions with more effective use of experimental budgets. The evolved SCMs also transfer across base models, suggesting reusable scientific knowledge beyond any single model's reasoning process.

The Relativity of Causal Knowledge (RCK) explains how a network of agents with different structural causal models can exchange causal knowledge through a shared interventionally consistent abstraction, or backbone. We ask the prior identification question that this transport mechanism presupposes: when is that backbone determined by the agents' private causal knowledge? In the basic two-agent common-effect case, two private causes influence one shared outcome and each agent identifies only the single-cause causal marginal relevant to its own perspective. We show that, under standard compatibility, non-degeneracy, and local overlap assumptions, those local causal marginals do not identify a unique backbone. Infinitely many joint intervention kernels can induce exactly the same private reports while disagreeing on joint interventions. We then give a conditional recovery result. Additive separability removes the hidden interaction degree of freedom, but observational residual summaries remain insufficient. Identification becomes possible when agents communicate causally identified response functions. An education value-added example illustrates why this is first a communication problem, and only then a policy-composition problem.

Hospital quality improvement (QI) programs routinely face multiple candidate interventions to optimize hospital flow, but existing methods struggle to estimate and rank the causal effects of such interventions. This work focuses on one of the most standard hospital metrics, the average length of stay (LOS), and its causal estimand, the average time saved. To characterize this causal effect, qualitative approaches rely on expert judgment to map patient trajectories, making them susceptible to cognitive biases; quantitative approaches rely on data-driven models, which fail when interventions are hypothetical with no historical data or have complex causal mechanisms that require clinical reasoning rather than data alone. We propose expert-guided g-computation, or egg-computation, which combines the complementary strengths of both approaches by connecting the Gantt charts commonly used to map patient trajectories with the causal DAG literature. We introduce a causal model over Gantt charts and establish identification using a variant of g-computation that seeks expert input only for components unidentifiable from data. To make egg-computation practical, we develop an LLM-assisted pipeline that reliably scales up expert reasoning. In simulations, egg-computation outperforms conventional causal inference methods when patients have diverse causal structures and intervention mechanisms. In a study of eleven candidate QI interventions at an urban safety-net hospital, the LLM pipeline generated graphs and time-saving estimates highly concordant with those of human experts. Beyond healthcare, egg-computation is a broadly applicable framework for estimating the average time saved for candidate interventions whose causal mechanisms can be represented using Gantt charts.

Generative models can reproduce an observational distribution while encoding an incorrect causal structure. We study a sequential game in which a structural causal generator proposes observational and interventional distributions, while an adversarial experimentalist selects interventions intended to maximally falsify the generator. The discriminator is therefore not merely a real-versus-synthetic classifier: it is indexed by an intervention and tests whether the generator reproduces the corresponding post-intervention law. We introduce Adversarial Causal Intervention Falsification (ACIF), formulate oracle and implementable versions of the game, and distinguish three objects that are often conflated: observational fit, interventional equivalence over an admissible query class, and point identification of a structural causal model. For finite model and intervention classes, we prove: (i) an exact reduction of the adversarial objective to a worst-intervention integral probability metric; (ii) identification up to interventional equivalence, with point identification under a separating intervention family; (iii) existence of mixed-strategy equilibria; (iv) finite-sample uniform convergence and margin-based model-selection guarantees; and (v) a logarithmic elimination guarantee for a disagreement-driven sequential design under a balanced-separation condition. We also give a complete linear-Gaussian example in which two observationally indistinguishable causal directions are separated by a single well-chosen intervention. The framework clarifies what an adversarial causal discriminator can and cannot certify, and provides a principled bridge between causal generative modeling, active causal discovery, and experimental design.

Causal perception occurs when agents with competing Structural Causal Models (SCMs) of the same system infer different probability distributions, including the hypothetical distributions implied by each agent's SCM under the same set of interventions. It shapes how agents reason about the system and how they perceive its fairness. Causal perception is a promising probabilistic framework, but it has remained purely theoretical. This work provides the first implementation of the causal perception framework of Álvarez and Ruggieri (2025). We operationalize structural (agents disagree on the causal graph) and parametrical (agents agree on the causal graph but disagree on its weights) causal perception. We design algorithms for computing interventional and counterfactual distributions and propose suitable distance measures to quantify the disagreement. Using the German Credit dataset, we illustrate how causal perception affects accuracy and fairness in a multi-expert decision setting. We show that the perception verdict is sensitive to the choice of distance metric and threshold. We also show that causal perception changes fairness assessments and threshold-based decisions. Bias proves situated with respect to the agent's SCM, demonstrating that competing worldviews in fairness problems cannot be ignored.

Counterfactual inference approaches for sequential decision-making typically assume deterministic causal models, where all randomness stems from latent variables. However, Markov Decision Processes (MDPs) are inherently stochastic. We address this by formalising counterfactual policy optimisation under probabilistic nondeterministic causal models, which properly separates latent confounding from irreducible stochasticity, and here propose a first practical optimisation problem for identifying robust counterfactual policies under a sensitivity analysis framework. We validate our approach on a sepsis treatment simulator, where diabetes status acts as a hidden global confounder.

Structural causal models are the standard language for reasoning about interventions and counterfactuals, but they describe static variables, typically measured once, and usually forbid cyclic dependencies. Many systems we care about, such as patients, climates, and economies, instead evolve continuously in time, are observed at irregular time points, and contain feedback loops. We argue that neural operator learning provides a natural foundation for causal reasoning in this setting, and propose Orca, a framework in which each node of the causal graph is a function of time and each mechanism is a learned map between function spaces. We extend existing neural operator architectures to express causal mechanisms: a mechanism computes the function value of a node from its parent nodes by taking several parent functions as input, respects the arrow of time, and treats latent exogenous noise as a function that can be inferred and reused for counterfactuals. We formalize the model class and demonstrate counterfactual reasoning on synthetic continuous-time examples. Code is available at https://github.com/gerritgr/orca

Most benchmarks for causal inference over time series are observational, small, or domain-specific, leaving interventional and counterfactual estimation under-served exactly where it matters most, such as in healthcare, policy evaluation, and climate science. We introduce \textbf{DoTime}, an open, scalable, and theoretically grounded generator of multivariate temporal structural causal models (TSCMs) with interventions, released as the \code{dotime} PyPI package together with four frozen evaluation suites. Beyond existing work, it adds capabilities absent from prior generators: continuous-time intervention \emph{windows}, counterfactual sampling modes with a positivity guard, regime-switching SCMs as a strict generalization of interrupted time series, non-stationary dynamics by construction with switching SCM parameters, and deterministic ramp and sinusoidal intervention profiles that place trends and structural breaks \emph{inside} the evaluation window. Moreover, it demonstrates the suitability of the generator as a prior for a causal foundation model reference implementation. The released suites span a training-scale snapshot of $100{,}000$ trajectories and eight named identification structures, each with exact ground truth: paired interventional trajectories from the same SCM throughout, and shared-noise counterfactuals in the continuous-time suite. We ship reference baseline implementations with an evaluation harness, and pose a falsifiable claim: interventional training buys a measurable direction-accuracy advantage over an observational model of identical capacity. It is tested across three training seeds per arm. Under structure-matched evaluation on held-out episodes, the interventional prior-fitted network's (PFN) gap is positive in every structure, trajectory length, and seed tested.

Predicting cellular responses to unseen chemical perturbations is challenging due to unknown targets and mechanisms, high-dimensional expression responses, and limited experimental coverage of the large small-molecule design space. We propose PerturbPFN, a PFN-style amortized model for unknown-target perturbation prediction under a hierarchical synthetic structural prior. Instead of directly regressing high-dimensional expression responses, PerturbPFN infers a latent system graph, sparse atomic intervention targets, and intervention strengths, then propagates their effects through an SCM decoder. The model is trained entirely on prior-predictive synthetic episodes generated from biologically motivated graph and expression simulators, enabling structured in-context learning without test-time gradient updates. We evaluate PerturbPFN on both real single-cell perturbation data and synthetic benchmarks, covering effect prediction, target identification, and regulatory structure discovery. Our results show that PerturbPFN offers a complementary trade-off to specialized baselines, achieving competitive perturbation prediction with low inference cost while exposing interpretable intermediate estimates of targets, strengths, and system structure.

Pearl's structural causal model (SCM) framework, built on directed acyclic graphs (DAGs) and the do-calculus, is the dominant formal language for causal reasoning. Yet it carries two structural restrictions: every relationship must be pre-specified as a directed causal edge, and feedback cycles are forbidden. This paper examines two classes of phenomena that strain these restrictions. First, symmetric physical and economic constraints, the ideal gas law being the canonical case, carry no intrinsic causal direction. Direction emerges only under intervention, and which variable is solved for must be specified as part of the intervention. We formalize such constraints as causal zeros within an Extended Causal Model by adding an activation operator, subject to local solvability and graph-admissibility conditions. Second, for the class of finite-propagation state-space systems considered here, we treat apparent instantaneous cycles as artifacts of suppressed time and ground both causal zeros and feedback in Causal Differential Equations (CDEs). In these, the transient regime is a time-unrolled acyclic causal process, and causal zeros arise as the defining functions of attracting equilibrium manifolds; periodic and chaotic attractors define further regimes of the same dynamics, treated through attractor-relative intervention. We give the extended do-calculus, identifiability conditions, counterfactual semantics, and open problems.

Estimating contemporaneous bidirectional interactions from observational data is difficult because each outcome is endogenous to the other, while flexible regressions may capture only reduced-form dependence. This paper proposes SEM-DNN, a heteroscedastic neural simultaneous-equation estimator that learns reciprocal structural interactions without external instruments. Identification exploits conditional covariance diagonalization: when structural shocks have zero conditional means, are conditionally uncorrelated given predetermined covariates, and exhibit nonproportional conditional variances, only the true interaction coefficients diagonalize the conditional residual covariance across the feature space. The method jointly approximates nonlinear structural mean functions and feature-dependent variances using a diagonal Gaussian quasi-likelihood that incorporates the simultaneous-system Jacobian. We establish unique identification and positive-definite local curvature of the profiled population criterion and show that, under neural-profile compatibility conditions, the implemented neural criterion inherits this curvature despite nonunique network parameterizations. The coefficients admit a causal interpretation when the structural equations represent autonomous mechanisms that remain invariant under the relevant interventions. Monte Carlo experiments with nonlinear, high-dimensional nuisance functions and non-Gaussian shocks show that SEM-DNN recovers structural effects more reliably than parametric, kernel-based, and separate-equation neural alternatives as information increases, although at greater computational cost. An application to ready-to-eat cereal scanner data illustrates how the method can study contemporaneous price-sales feedback and assess identification strength, residual diagonalization, variance calibration, and optimization sensitivity.

Let $p(x)$ be the joint density of variables $X$, and let $ψ(x)=\nabla_x\log p(x)$ be its score field. Geometry constructed from $p$ and $ψ$ alone cannot identify causal direction: structural models with the same observational distribution have the same score geometry. I develop an interventional analogue. A hard intervention $\operatorname{do}(X_k=ξ)$ does not merely reweight the joint law; it restricts the distribution to the submanifold ${x_k=ξ}$. Its score should therefore be defined on the remaining $d-1$ free coordinates. I define causal influence $X_k\rightsquigarrow X_j$ as variation of the interventional marginal distribution of $X_j$ with $ξ$, and show that the corresponding derivative of the marginal interventional score gives a local sufficient condition for influence. Projecting the observational score onto admissible intervention directions does not generally recover causal response: two models may share the same observational score and admissible set yet respond differently. I therefore introduce an interventional response field supplied by structural information. A causal metric is defined as the Fisher information metric on a family of interventions with a common target, avoiding ill-posed comparisons across targets. The framework yields a geometric dictionary for randomized trials, instrumental variables, and conditional-independence designs, clarifying what each does and does not identify. A bivariate Gaussian example gives two models with the same observational score but different interventional score derivatives. The framework organizes relations among designs, interventions, and score fields, but adds no identification beyond the underlying assumptions. In Pearl's Ladder of Causation, observational score geometry belongs to association, intervention-indexed score fields to intervention, and unit-level counterfactual geometry is left for future work.

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

We formalize verification in causal graphical models: deciding whether a given observational formula identifies a target interventional distribution. This opens a problem complementary to identification, asking not whether any identifying formula exists, but whether the given formula is identifying. We show that even sound and complete solutions to identification do not solve verification. We propose a falsifier as a first practical route forward, prove that it induces an almost-surely correct verifier for regular exponential-family models, and use the resulting verifier to develop the gateway test, which finds all sets admissible for use in a front-door formula.

Causal discovery from observational tabular data remains fundamentally challenging, primarily due to the heterogeneity of underlying causal mechanisms and the high-dimensional combinatorial search space of Directed Acyclic Graphs (DAGs). In this paper, we propose \textbf{DAG-FM}, a novel foundation model architecture that amortizes causal discovery. Unlike direct matrix prediction, DAG-FM decomposes the causal discovery process into two auto-regressive stages using two specialized Transformer-based sub-modules: a leaf-node predictor and a parent-node predictor. To effectively model complex row-column interactions, we adopt a robust tabular interaction block to output feature-wise representations. Crucially, to handle diverse and unknown Functional Causal Model (FCM) assumptions in real-world scenarios, we introduce Mixture-of-Leaf-Experts (MoLE), allowing the model to dynamically route and adapt to identifiable mechanism families. Through an iterative inference algorithm, DAG-FM seamlessly extracts causal orderings and constructs valid DAGs. Extensive experiments demonstrate that DAG-FM achieves state-of-the-art performance on both synthetic benchmarks and complex real-world datasets, significantly outperforming traditional classical algorithms and recent foundation models in both accuracy and scalability.

Bayesian causal discovery is widely used for its ability to quantify epistemic uncertainty over directed acyclic graphs (DAGs) through posterior inference. However, its behaviour under latent confounding remains poorly understood, as existing work typically notes that confounding breaks identifiability without characterising how the posterior distribution over DAGs responds. In this work, we analyse posterior behaviour under latent confounding in linear Gaussian causal models, focusing on additive latent confounding between exactly two observed variables. We derive a critical correlation threshold above which the score function favours graphs with a spurious edge between the confounded variables, and show that this threshold decreases with sample size -- more data lowers the correlation required for the spurious edge to be favoured. Beyond this threshold, we characterize two distinct posterior failure regimes determined by the local structure around the confounded variables. Our findings are supported by exact posterior computations on multiple graph structures, demonstrating both the predicted failure regimes.

Large language models (LLMs) increasingly act as integrated data-science agents, combining abstract reasoning with advanced tool use. Yet the relevant benchmark landscape largely divides into symbolic causal reasoning benchmarks without realistic data analysis or data analysis benchmarks without a principled causal data-generating structure. Furthermore, existing causal evaluation datasets are often restricted to curated examples from existing sources, with diversity coming from limited templatized variations rather than from systematic generation of novel synthetic causal structures. We introduce CausalDS, a benchmark for evaluating causal reasoning in agentic data-science workflows. Each benchmark instance is a scene consisting of a sampled structural causal model (SCM) with generated observational data and an accompanying synthetic natural-language story grounded in a realistic domain. We optionally ground the composition of the benchmark components in empirical distributions obtained from real-world datasets, thus retaining empirical structure while reducing the "causal parrot" risk through completely synthetic generation. From each scene, we then derive tasks spanning all three of Pearl's rungs, with typical data-science prediction tasks appearing as Rung 1. Most tasks include a data science coding component, where the model typically needs to use several tools to arrive at the final answer due to the frequent presence of imperfect observations, which are generated by an observation model. Additionally, recognizing when a question admits no warranted answer and abstaining is treated as a first-class scored outcome. The benchmark thus jointly evaluates symbolic causal reasoning, data science, uncertainty quantification, abstention, and tool use/coding.

Recovering the exact directed acyclic graph (DAG) in linear non-Gaussian acyclic models with latent confounders (LvLiNGAM) remains a challenging problem. Although LvLiNGAM is identifiable only up to an observational equivalence class, each equivalence class is characterized by a unique sparsest DAG. Recovering the sparsest DAG from finite samples, however, remains difficult. Although existing methods are asymptotically consistent, they do not provide an explicit finite-sample procedure for recovering the unique sparsest DAG, nor do they handle models with an arbitrary number of latent confounders. In this paper, we propose a finite-sample method for recovering the sparsest DAG without imposing any restriction on the number of latent confounders. Simulation studies and real-data analyses demonstrate that the proposed method achieves superior finite-sample performance compared with existing approaches.