Understanding potential selection in data is crucial for causal discovery; we argue that "selection" in common narratives takes two forms, which we term static and evolutionary selection, respectively. Static selection refers to a one-shot filtering process where observed data consist of a subset of the population of interest, as in survey volunteer bias. Evolutionary selection, in contrast, operates through repeated rounds of differential fitness in reproduction, where observed data constitute the latest generation shaped by a historical trajectory, as in immune adaptation, antibiotic resistance, and social norm emergence. Existing methods largely conflate these two forms and rely on an identical graphical model of selection. We show that this model is valid for static settings but fails to characterize data under evolution, yielding false discovery results. To address this, we introduce a new model that specifically characterizes evolutionary selection, and develop a sound and complete procedure for identifying such models from data across one or multiple environments or generations. Experimental results validate the method's ability to uncover the relevant mechanisms underlying evolution from data.
Causal discovery methods commonly assume that all data is independently and identically distributed (i.i.d.) and that there are no unmeasured variables affecting the system. In practice, these assumptions are often violated, leading to inaccurate inference. In this paper, we study how to identify hidden confounding and selection biases from causal mechanism shifts. In particular, we show that structural biases lead to dependent mechanism shifts. That is, by considering for which variables the mechanisms change given data from different environments, we can tell which variables are unbiased, which are subject to hidden confounding, and which are undergoing selection bias. We formalize this into an empirically testable criterion based on mutual information, and show under which conditions it identifies structural biases. To tell which nodes are subject to what kind of bias, we introduce the StruBI algorithm. Experiments on synthetic and real-world data show that StruBI works well in practice, accurately recovering affected variable sets and types of biases, outperforming the state-of-the-art by a wide margin.
Praharsh Nanavati, Jilles Vreeken, David Kaltenpoth
Modern machine learning models excel at pattern recognition but remain brittle, often failing to generalize out of distribution (OOD) because they capture spurious correlations rather than the underlying causal data-generating process. Current causal discovery methods, while powerful, typically assume a static graph structure, rendering them unable to model systems that adapt or undergo structural changes across different environments. We introduce ECR-Net, Evolving Causal Regulatory Networks, a novel, bio-inspired framework for adaptive causal mechanism discovery. Our approach models the data-generating process not as a static graph, but as a dynamic system analogous to a Gene Regulatory Network (GRN), composed of localized, recursive functions where variables can activate and inhibit one another. To discover the latent structure of this network, we employ an evolutionary search algorithm that evolves a population of candidate regulatory graphs, optimizing for a fitness function that measures how well the simulated system dynamics reconstruct the observed data. The key innovation of ECR-Net is its ability to model structural adaptation, it explicitly ingests shifts in the data's statistical properties as signals of an environmental shock. In response, the evolutionary search identifies parsimonious modifications to the causal graph topology, such as link inhibitions or activations that explain the new data regime. We posit that ECR-Net represents a new class of adaptive Structural Causal Models capable of discovering how and why a system's fundamental rules change, offering a path toward robust generalization in complex, non-stationary systems.
Govind Vallabhasseri Binish, Abdhul Ahadh, Rano Roy Kavanal +1
Selection bias is pervasive in observational studies. For example, large scale biobanks data can exhibit ``healthy volunteer bias'' when respondents are healthier and of higher socio-economic status than the population they are meant to represent. Recovering causal effects from such sub-population is an important problem in causal inference, as estimating average treatment effects (ATE) from selected populations can result in a severely biased estimate of the ATE from the whole population. In this paper, we investigate the identifiability of the ATE under selection bias. We provide necessary and sufficient conditions for ATE identifiability, leveraging weak assumptions on probability classes to characterize propensity score and selection probability. Compared to previous works, our results extend existing graphical identifiability criteria and offer a more comprehensive understanding of causal effect identification with strictly weaker conditions in the presence of selection bias.