Causal discovery, the problem of inferring the direction of causality, is generally ill-posed. We use the language of structural causal models (SCM) to show that assuming that the causal relations are acyclic and invariant across multiple environments (e.g., the way minimum wage affects employment rate is stable across different geographical regions), \textit{only} two auxiliary environments are sufficient to infer the causal graph for arbitrary nonlinear mechanisms. Moreover, we demonstrate that this implies identifiability of the SCM functional mechanisms: as a corollary, we show that \textit{two} auxiliary environments are sufficient to guarantee correct counterfactual inference. We empirically support our theoretical results on synthetic data.

The trustworthiness of AI decision-making systems is increasingly important. A key feature of such systems is the ability to provide recommendations for how an individual may reverse a negative decision, a problem known as algorithmic recourse. Existing approaches treat recourse outcomes as counterfactuals of a fixed unit, ignoring that real-world recourse involves repeated decisions on the same individual under possibly different latent conditions. We develop a causal framework that models recourse as a process over pre- and post-intervention outcomes, allowing for partial stability and resampling of latent variables. We introduce post-recourse stability conditions that enable reasoning about recourse from observational data alone, and develop a copula-based algorithm for inferring the effects of recourse under these conditions. For settings where paired observations of the same individual before and after intervention are available (called recourse data), we develop methods for inferring copula parameters and performing goodness-of-fit testing. When the copula model is rejected, we provide a distribution-free algorithm for learning recourse effects directly from recourse data. We demonstrate the value of the proposed methods on real and semi-synthetic datasets.

Despite theoretical advantages, causal methods for Gene Regulatory Network (GRN) inference from single-cell RNA-seq data consistently fail to match or outperform correlation-based baselines in many realistic benchmarks, a persistent puzzle which casts doubt on the value of causality for this task. We argue that existing benchmarks are insufficiently controlled to answer this question because they evaluate on real or semi-real data where multiple pathologies co-occur, confounding failure modes, and obscuring the specific conditions under which different inference methods excel or fail. To address this gap, we introduce a controlled diagnostic framework that isolates seven biologically motivated pathologies (dropout, latent confounders, cell-type mixing, feedback loops, network density, sample size, and pseudotime drift) and measure how six representative methods spanning three inference paradigms degrade as each pathology intensifies. Across 6,120 controlled experiments, we find that causal methods genuinely dominate in clean and structurally favorable regimes, but specific pathologies (notably dropout and latent confounders) selectively neutralize their advantages. We further introduce an errortype decomposition that reveals methods with similar aggregate accuracy commit qualitatively different errors. To probe whether single-pathology effects persist when multiple stressors co-occur, we perform an interaction sweep over the three most impactful pathologies and find that their joint effects are sub-additive, while also exposing density-conditional cross-overs invisible to single-dial analysis. Our findings offer a nuanced understanding of when and why different methods succeed or fail for GRN inference, providing actionable insights for method development and practical guidance for practitioners.3

Symbol Description Vt Set of observable variables at time t V0:TUnion of observable variables at time t= 0,...,T Xt Manipulative variables at time t Yt Target variable at time t P(Xt) Power set of Xt Mt Set of MIS sets at time t Xs,ts-th intervention set at time t In this section we give the proof for Theorem 1 in the main text. This means that W includes those variables that are parents of Yt but are nor target at previous time steps nor intervened variables. In the following proof the values of IV0:t 1, XPYs,t, IPY0:t 1 and W are denoted by i, xPY, iPY and w respectively. Finally, fYY and fNYYare the functions in the SCM for Yt (see Assumptions (1) in the main text). Eq. (2) follows from the Eq. Finally, noticing that p(yPTt |I0:t 1) is the distribution targeted when optimizing the objective function at previous time steps one can obtain Eq. (6). The derivations above show how the objective function at time t is given by the expected value of the output of the functional relationship fNYYwhere the expectation is taken with respect to the variables that are not intervened on. This expectation is then shifted to account for the interventions implemented in the system at previous time steps that are affecting the target variable through fYY .

Combination therapy refers to the use of multiple treatments - such as surgery, medication, and behavioral therapy - to cure a single disease, and has become a cornerstone for treating various conditions including cancer, HIV, and depression. All possible combinations of treatments lead to a collection of treatment regimens (i.e., policies) with mixed scopes, or what physicians could observe and which actions they should take depending on the context. In this paper, we investigate the online reinforcement learning setting for optimizing the policy space with mixed scopes. In particular, we develop novel online algorithms that achieve sublinear regret compared to an optimal agent deployed in the environment. The regret bound has a dependency on the maximal cardinality of the induced state-action space associated with mixed scopes. We further introduce a canonical representation for an arbitrary subset of interventional distributions given a causal diagram, which leads to a non-trivial, minimal representation of the model parameters.

Our results are corroborated with experiments.

RCM. Finally, we illustrate the power of this conciliatory perspective by pinpointing

Thus, becoming convoluted and difficult to analyze.