Graphical models have been widely used as parsimonious encoders of assumptions of the underlying causal system and provide a basis for causal inferences. Models encoding stronger constraints tend to require higher expressive power, which are also harder, and sometimes impossible to empirically falsify. In this paper, we introduce two new collections of distributions that include counterfactual quantities which are experimentally accessible under counterfactual randomizations. Correspondingly, we define two new classes of graphical models for encoding empirically testable constraints in these distributions. We further present a sound and complete calculus, based on counterfactual calculus, which licenses inferences in these two new models with rules that are within the empirically falsifiable boundary. Finally, we formulate a hierarchy over several graphical models based on the constraints they encode and study the fundamental trade-off between the expressive power and empirical falsifiability of different models across the hierarchy.

Most counterfactual inference frameworks traditionally assume acyclic structural causal models (SCMs), i.e. directed acyclic graphs (DAGs).

Deep neural networks have been criticized as fundamentally statistical systems that fail to capture causal structure and perform causal reasoning. Here we demonstrate that a GPT-style transformer trained for next-token prediction can simultaneously discover instances of linear Gaussian structural causal models (SCMs) and learn to answer counterfactual queries about those SCMs. First, we show that the network generalizes to counterfactual queries about SCMs for which it has seen interventional data but not any examples of counterfactual inference. The network must, thus, have successfully composed discovered causal structures with a learned counterfactual inference algorithm. Second, we decode the implicit "mental" SCM from the network's residual stream activations and manipulate it using gradient descent with predictable effects on the network's output. Our results suggest that statistical prediction may be sufficient to drive the emergence of internal causal models and causal inference capacities in deep neural networks.

Warning: this paper may contain potentially generated harmful content. Though safety alignment has been applied to most large language models (LLMs), LLM service providers generally deploy a subsequent moderation as the external safety guardrail in real-world products. Existing moderators mainly practice a conventional full detection, which determines the harmfulness based on the complete LLM output, causing high service latency. Recent works pay more attention to partial detection where moderators oversee the generation midway and early stop the output if harmfulness is detected, but they directly apply moderators trained with the full detection paradigm to incomplete outputs, introducing a training-inference gap that lowers the performance. In this paper, we explore how to form a data-andmodel solution that natively supports partial detection. For the data, we construct FineHarm, a dataset consisting of 29K prompt-response pairs with fine-grained token-level annotations to provide reasonable supervision for token-level training. Then, we propose the Streaming Content Monitor (SCM), which is trained with dual supervision of response-and token-level labels and can follow the output stream of LLM to make a timely judgment of harmfulness. Experiments show that SCM gains 0.95+ in macro F1 score that is comparable to full detection, by only seeing the first 18% of tokens in responses on average. Moreover, the SCM can serve as a pseudo-harmfulness annotator for improving safety alignment and lead to a higher harmlessness score than DPO.

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.