Constraint-based causal discovery is widely used for learning causal structures, but heavy reliance on conditional independence (CI) testing makes it computationally expensive in high-dimensional settings. To mitigate this limitation, many divide-and-conquer frameworks have been proposed, but most assume causal sufficiency, i.e., no latent variables. In this paper, we show that divide-and-conquer strategies can be theoretically generalized beyond causal sufficiency to settings with latent variables. Specifically, we propose a recursive decomposition framework, termed DiCoLa, that enables divide-and-conquer causal discovery in the presence of latent variables. It recursively decomposes the global learning task into smaller subproblems and integrates their solutions through a principled reconstruction step to recover the global structure. We theoretically establish the soundness and completeness of the proposed framework. Extensive experiments on synthetic data demonstrate that our approach significantly improves computational efficiency across a range of causal discovery algorithms, while experiments on a real-world dataset further illustrate its practical effectiveness.

Dataset bias often leads deep learning models to exploit spurious correlations instead of task-relevant signals. We introduce the Standard Anti-Causal Model (SAM), a unifying causal framework that characterizes bias mechanisms and yields a conditional independence criterion for causal stability. Building on this theory, we propose DISCO$_m$ and sDISCO, efficient and scalable estimators of conditional distance correlation that enable independence regularization in gradient-based models. Across six diverse datasets, our methods consistently outperform or are competitive in existing observed bias mitigation approaches, while requiring fewer hyperparameters and scaling seamlessly to multi-bias scenarios. This work bridges causal theory and practical deep learning, providing both a principled foundation and effective tools for robust prediction. Source Code: https://github.com/yakamoz5/DISCO.

Electronic health records (EHR) pose large-scale multi-disease modeling problems in which many outcomes are rare and strongly influenced by shared risk factors. While modern approaches achieve strong predictive performance, they often treat diseases independently or rely on black-box architectures, offering limited insight into how risk factors organize disease risk and little principled uncertainty quantification. We introduce a Bayesian hypergraph inference framework that reframes multi-disease modeling around latent, risk-factor-modulated disease pathways. Risk factors act on hyperedges, latent disease subsets with shared risk patterns, allowing diseases to participate in multiple distinct pathways and enabling interpretable, higher-order structure beyond pairwise associations. A repulsion prior encourages parsimonious and identifiable structure, while posterior inference provides calibrated uncertainty over both disease groupings and risk-factor influence. To enable scalable inference on large EHR datasets, we develop a structured variational inference algorithm that preserves logical dependencies among hyperedge existence, disease membership, and pathway-level effects. Experiments on simulated data and UK Biobank demonstrate stable and interpretable disease pathway structure, well-calibrated uncertainty, improved estimation for rare diseases, and competitive predictive performance.

Causal discovery from observational count data poses unique challenges, particularly when the data exhibit inherent branching structures, such as an upstream ad impression event triggering a downstream purchase event with certain probability. Such branching dynamics are naturally modeled by thinning operators (for branching) and an independent Poisson distribution (for exogenous noise), constituting a Poisson Branching Structural Causal Model (PB-SCM). However, existing approaches based on PB-SCM rely on the restrictive assumption of causal sufficiency, failing to account for ubiquitous latent confounders. In this work, we propose a Latent Confounding Poisson Branching Structural Causal Model (LC-PB-SCM) to bridge this gap. We leverage Probability Generating Function (PGF) to characterize the complex dependencies introduced by latent confounding. Then, we establish a Trie representation theorem that maps the branching structure to algebraic properties of PGF monomials. Based on local PGF, we establish a complete identifiability condition for local 3-variables covering all causal patterns distinguishable up to monomial equivalence. Finally, we propose a practical algorithm to learn causal structures under latent confounding and demonstrate its effectiveness through experiments on both synthetic and real-world datasets.