Efficient Discovery of Approximate Causal Abstractions via Neural Mechanism Sparsification

Neural networks are hypothesized to implement interpretable causal mechanisms, yet verifying this requires finding a causal abstraction -- a simpler, high-level Structural Causal Model (SCM) faithful to the network under interventions. Discovering such abstractions is hard: it typically demands brute-force interchange interventions or retraining. We reframe the problem by viewing structured pruning as a search over approximate abstractions. Treating a trained network as a deterministic SCM, we derive an Interventional Risk objective whose second-order expansion yields closed-form criteria for replacing units with constants or folding them into neighbors. Under uniform curvature, our score reduces to activation variance, recovering variance-based pruning as a special case while clarifying when it fails. The resulting procedure efficiently extracts sparse, intervention-faithful abstractions from pretrained networks, which we validate via interchange interventions.

Coarse-to-Fine Learning of Dynamic Causal Structures

Learning the dynamic causal structure of time series is a challenging problem. Most existing approaches rely on distributional or structural invariance to uncover underlying causal dynamics, assuming stationary or partially stationary causality. However, these assumptions often conflict with the complex, time-varying causal relationships observed in real-world systems. This motivates the need for methods that address fully dynamic causality, where both instantaneous and lagged dependencies evolve over time. Such a setting poses significant challenges for the efficiency and stability of causal discovery. To address these challenges, we introduce DyCausal, a dynamic causal structure learning framework. DyCausal leverages convolutional networks to capture causal patterns within coarse-grained time windows, and then applies linear interpolation to refine causal structures at each time step, thereby recovering fine-grained and time-varying causal graphs. In addition, we propose an acyclic constraint based on matrix norm scaling, which improves efficiency while effectively constraining loops in evolving causal structures. Comprehensive evaluations on both synthetic and real-world datasets demonstrate that DyCausal achieves superior performance compared to existing methods, offering a stable and efficient approach for identifying fully dynamic causal structures from coarse to fine.

Empirically Calibrated Conditional Independence Tests

Conditional independence tests (CIT) are widely used for causal discovery and feature selection. Even with false discovery rate (FDR) control procedures, they often fail to provide frequentist guarantees in practice. We highlight two common failure modes: (i) in small samples, asymptotic guarantees for many CITs can be inaccurate and even correctly specified models fail to estimate the noise levels and control the error, and (ii) when sample sizes are large but models are misspecified, unaccounted dependencies skew the test's behavior and fail to return uniform p-values under the null. We propose Empirically Calibrated Conditional Independence Tests (ECCIT), a method that measures and corrects for miscalibration. For a chosen base CIT (e.g., GCM, HRT), ECCIT optimizes an adversary that selects features and response functions to maximize a miscalibration metric. ECCIT then fits a monotone calibration map that adjusts the base-test p-values in proportion to the observed miscalibration. Across empirical benchmarks on synthetic and real data, ECCIT achieves valid FDR with higher power than existing calibration strategies while remaining test agnostic.

Fast Flow Matching based Conditional Independence Tests for Causal Discovery

Constraint-based causal discovery methods require a large number of conditional independence (CI) tests, which severely limits their practical applicability due to high computational complexity. Therefore, it is crucial to design an algorithm that accelerates each individual test. To this end, we propose the Flow Matching-based Conditional Independence Test (FMCIT). The proposed test leverages the high computational efficiency of flow matching and requires the model to be trained only once throughout the entire causal discovery procedure, substantially accelerating causal discovery. According to numerical experiments, FMCIT effectively controls type-I error and maintains high testing power under the alternative hypothesis, even in the presence of high-dimensional conditioning sets. In addition, we further integrate FMCIT into a two-stage guided PC skeleton learning framework, termed GPC-FMCIT, which combines fast screening with guided, budgeted refinement using FMCIT. This design yields explicit bounds on the number of CI queries while maintaining high statistical power. Experiments on synthetic and real-world causal discovery tasks demonstrate favorable accuracy-efficiency trade-offs over existing CI testing methods and PC variants.

CauScale: Neural Causal Discovery at Scale

Causal discovery is essential for advancing data-driven fields such as scientific AI and data analysis, yet existing approaches face significant time- and space-efficiency bottlenecks when scaling to large graphs. To address this challenge, we present CauScale, a neural architecture designed for efficient causal discovery that scales inference to graphs with up to 1000 nodes. CauScale improves time efficiency via a reduction unit that compresses data embeddings and improves space efficiency by adopting tied attention weights to avoid maintaining axis-specific attention maps. To keep high causal discovery accuracy, CauScale adopts a two-stream design: a data stream extracts relational evidence from high-dimensional observations, while a graph stream integrates statistical graph priors and preserves key structural signals. CauScale successfully scales to 500-node graphs during training, where prior work fails due to space limitations. Across testing data with varying graph scales and causal mechanisms, CauScale achieves 99.6% mAP on in-distribution data and 84.4% on out-of-distribution data, while delivering 4-13,000 times inference speedups over prior methods. Our project page is at https://github.com/OpenCausaLab/CauScale.

Causal Cellular Context Transfer Learning (C3TL): An Efficient Architecture for Prediction of Unseen Perturbation Effects

Predicting the effects of chemical and genetic perturbations on quantitative cell states is a central challenge in computational biology, molecular medicine and drug discovery. Recent work has leveraged large-scale single-cell data and massive foundation models to address this task. However, such computational resources and extensive datasets are not always accessible in academic or clinical settings, hence limiting utility. Here we propose a lightweight framework for perturbation effect prediction that exploits the structured nature of biological interventions and specific inductive biases/invariances. Our approach leverages available information concerning perturbation effects to allow generalization to novel contexts and requires only widely-available bulk molecular data. Extensive testing, comparing predictions of context-specific perturbation effects against real, large-scale interventional experiments, demonstrates accurate prediction in new contexts. The proposed approach is competitive with SOTA foundation models but requires simpler data, much smaller model sizes and less time. Focusing on robust bulk signals and efficient architectures, we show that accurate prediction of perturbation effects is possible without proprietary hardware or very large models, hence opening up ways to leverage causal learning approaches in biomedicine generally.

Traceable Latent Variable Discovery Based on Multi-Agent Collaboration

Revealing the underlying causal mechanisms in the real world is crucial for scientific and technological progress. Despite notable advances in recent decades, the lack of high-quality data and the reliance of traditional causal discovery algorithms (TCDA) on the assumption of no latent confounders, as well as their tendency to overlook the precise semantics of latent variables, have long been major obstacles to the broader application of causal discovery. To address this issue, we propose a novel causal modeling framework, TLVD, which integrates the metadata-based reasoning capabilities of large language models (LLMs) with the data-driven modeling capabilities of TCDA for inferring latent variables and their semantics. Specifically, we first employ a data-driven approach to construct a causal graph that incorporates latent variables. Then, we employ multi-LLM collaboration for latent variable inference, modeling this process as a game with incomplete information and seeking its Bayesian Nash Equilibrium (BNE) to infer the possible specific latent variables. Finally, to validate the inferred latent variables across multiple real-world web-based data sources, we leverage LLMs for evidence exploration to ensure traceability. We comprehensively evaluate TLVD on three de-identified real patient datasets provided by a hospital and two benchmark datasets. Extensive experimental results confirm the effectiveness and reliability of TLVD, with average improvements of 32.67% in Acc, 62.21% in CAcc, and 26.72% in ECit across the five datasets.

CausalCompass: Evaluating the Robustness of Time-Series Causal Discovery in Misspecified Scenarios

Causal discovery from time series is a fundamental task in machine learning. However, its widespread adoption is hindered by a reliance on untestable causal assumptions and by the lack of robustness-oriented evaluation in existing benchmarks. To address these challenges, we propose CausalCompass, a flexible and extensible benchmark suite designed to assess the robustness of time-series causal discovery (TSCD) methods under violations of modeling assumptions. To demonstrate the practical utility of CausalCompass, we conduct extensive benchmarking of representative TSCD algorithms across eight assumption-violation scenarios. Our experimental results indicate that no single method consistently attains optimal performance across all settings. Nevertheless, the methods exhibiting superior overall performance across diverse scenarios are almost invariably deep learning-based approaches. We further provide hyperparameter sensitivity analyses to deepen the understanding of these findings. We also find, somewhat surprisingly, that NTS-NOTEARS relies heavily on standardized preprocessing in practice, performing poorly in the vanilla setting but exhibiting strong performance after standardization. Finally, our work aims to provide a comprehensive and systematic evaluation of TSCD methods under assumption violations, thereby facilitating their broader adoption in real-world applications. The code and datasets are available at https://github.com/huiyang-yi/CausalCompass.

Effect-Level Validation for Causal Discovery

Causal discovery is increasingly applied to large-scale telemetry data to estimate the effects of user-facing interventions, yet its reliability for decision-making in feedback-driven systems with strong self-selection remains unclear. In this paper, we propose an effect-centric, admissibility-first framework that treats discovered graphs as structural hypotheses and evaluates them by identifiability, stability, and falsification rather than by graph recovery accuracy alone. Empirically, we study the effect of early exposure to competitive gameplay on short-term retention using real-world game telemetry. We find that many statistically plausible discovery outputs do not admit point-identified causal queries once minimal temporal and semantic constraints are enforced, highlighting identifiability as a critical bottleneck for decision support. When identification is possible, several algorithm families converge to similar, decision-consistent effect estimates despite producing substantially different graph structures, including cases where the direct treatment-outcome edge is absent and the effect is preserved through indirect causal pathways. These converging estimates survive placebo, subsampling, and sensitivity refutation. In contrast, other methods exhibit sporadic admissibility and threshold-sensitive or attenuated effects due to endpoint ambiguity. These results suggest that graph-level metrics alone are inadequate proxies for causal reliability for a given target query. Therefore, trustworthy causal conclusions in telemetry-driven systems require prioritizing admissibility and effect-level validation over causal structural recovery alone.

Physics as the Inductive Bias for Causal Discovery

Causal discovery is often a data-driven paradigm to analyze complex real-world systems. In parallel, physics-based models such as ordinary differential equations (ODEs) provide mechanistic structure for many dynamical processes. Integrating these paradigms potentially allows physical knowledge to act as an inductive bias, improving identifiability, stability, and robustness of causal discovery in dynamical systems. However, such integration remains challenging: real dynamical systems often exhibit feedback, cyclic interactions, and non-stationary data trend, while many widely used causal discovery methods are formulated under acyclicity or equilibrium-based assumptions. In this work, we propose an integrative causal discovery framework for dynamical systems that leverages partial physical knowledge as an inductive bias. Specifically, we model system evolution as a stochastic differential equation (SDE), where the drift term encodes known ODE dynamics and the diffusion term corresponds to unknown causal couplings beyond the prescribed physics. We develop a scalable sparsity-inducing MLE algorithm that exploits causal graph structure for efficient parameter estimation. Under mild conditions, we establish guarantees to recover the causal graph. Experiments on dynamical systems with diverse causal structures show that our approach improves causal graph recovery and produces more stable, physically consistent estimates than purely data-driven state-of-the-art baselines.