Reconciling Consistency-Based Diagnosis with Actual-Causality-Based Explanations

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.

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.

Explainable artificial intelligence (XAI) increasingly calls for actionable counterfactual recourse, yet current methodologies face challenges related to causal invalidity, excessive cognitive burden, and predictive failure. Exhaustive causal search algorithms often require modifications to multiple attributes, whereas additive attribution-guided methods, such as SHAP, ignore higher-order feature synergies, leading to suboptimal predictive momentum and diffuse intervention effort in complex nonlinear models, such as XGBoost. To bridge this gap, we introduce actionable case-based feature importance (A-CBFI), a diagnosis-prescription integrated framework for tabular machine learning. Grounded in structural causal models (SCMs), A-CBFI isolates synergistic interaction bottlenecks and releases suppressive structural locks, translating them into targeted interventions. By mathematically separating the active user intervention space (L_{\mathrm{active}}) from downstream effects and concentrating over 98.3% of the intervention effort on diagnosed root causes, A-CBFI enables highly targeted interventions. Empirical evaluations across the financial and healthcare domains demonstrate that A-CBFI reduces the active human intervention burden by 77.0% while maintaining comparable global recourse cost to exhaustive causal baselines. By prioritizing the diagnosed causal bottlenecks, A-CBFI provides targeted and actionable recourse while maintaining causal validity and achieving full relative convergence across all causally feasible instances.