Causal Discovery in Mixtures of Populations

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.

Causal discovery from observational data remains challenging due to the need to recover directed structure and latent confounding without interventions. We propose FoundCause, an amortized causal discovery model trained entirely on synthetic data that maps datasets directly to causal graphs in a single forward pass. By learning from large collections of simulated structural causal models, FoundCause captures transferable statistical patterns that generalize beyond individual datasets. The architecture incorporates several key inductive biases for causal discovery. It uses a permutation-invariant transformer encoder with alternating attention over samples and variables to jointly model cross-variable dependence and per-variable distributions. Pairwise statistical features derived from classical asymmetry measures are injected through statistics-conditioned attention, guiding the model toward known causal signals. A factorized decoder separates edge existence from direction, while a triangular refinement module enables reasoning over higher-order causal motifs such as chains and colliders. In addition, a dedicated confounder module based on learnable latent tokens explicitly models hidden common causes, and the model explicitly handles missing data via its masked input representation. To our knowledge, FoundCause is the first amortized causal discovery approach to explicitly model latent confounding. FoundCause outperforms 11 classical non-amortized methods (e.g., PC, GES, NOTEARS-style optimization) and 4 amortized causal discovery methods on 15 real-world datasets, achieving +9.6% improvement in $F_1$, +1.2% in AUROC, and an 18.9% reduction in structural Hamming distance relative to the strongest non-amortized methods, while performing inference in a single forward pass.

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.