Counterfactual identifiability beyond global monotonicity: non-monotone triangular structural causal models
Authors: Pengcheng Tan, Jiang Chen, Dehui Du
Organizations: Shanghai Key Laboratory of Trustworthy Computing, East China Normal University
Abstract
Structural causal models provide a unified semantics for interventions and counterfactuals, but most identifiability results rely on restrictive assumptions like global monotonicity, which are often violated in embodied interaction, where the same exogenous perturbation can induce opposite responses under different contact contexts. We ask what structure still suffices once global monotonicity is dropped. We introduce non-monotone triangular structural causal models (NM-TM-SCM), which retain triangular recursion but replace global monotonicity with mechanism-wise invertibility and context-independent inverse transport. We prove that these conditions are equivalent to exogenous isomorphism and imply complete counterfactual identifiability, and we give a counterexample showing that local invertibility alone is insufficient. We instantiate the theory in CausalInverter, with triangular invertible layers, orientation gates, and transport-stability regularization. On synthetic non-monotonic mechanisms, the structural bias yields systematic counterfactual gains as non-monotonicity increases. On MuJoCo Door, our model achieves perfect event-level counterfactual recovery, lowers continuous angle error relative to a Transformer baseline, and delivers substantially more stable recovery than Transformer and conditional-flow predictors. On MuJoCo Push, where non-monotonicity is weaker, the same low-data predictors remain competitive or better, consistent with a bias-variance boundary. These results identify a broader identifiable regime between globally monotone triangular models and unconstrained black-box world models.
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.
An artificial intelligence must have a model of its environment that is causal, supporting reasoning about interventions and counterfactuals, and also combinatorial, supporting generalization to unseen combinations of objects. In this work, we formally study when and how such a model can be learned. We develop relational structural causal models, extending structural causal models (Pearl 2009) to settings where objects and their relations vary. First, we show how answers to not only causal but also observational queries about unseen combinations of objects can not be identified without further assumptions. To enable such identification--including in the presence of unobserved confounding--we define relational causal graphs and derive symbolic identification criteria. Finally, we propose relational neural causal models, a provably correct approach that outperforms non-relational baselines on simulated traffic scenes with varying cars, signals, and pedestrians.
Here we introduce Partially Observed Structural Causal Models (POSCMs) as an extension of structural causal models (SCMs) to settings where upstream contexts co-determine both the interaction structure and downstream mechanisms on observed variables. POSCMs thus provide a self-contained causal modeling framework for endogenous graphs, allowing for an intervention hierarchy spanning node- and edge-level contexts and endogenous variable interventions. To define edge interventions, we separate node mechanisms into edge-local transmission channels that can be modified without changing the source node or the rest of the target mechanism. We provide an identifiability theory that clarifies which intervention families would suffice to disentangle structure formation from mechanisms. We then empirically validate these theoretical results in two external simulators: a biophysically detailed virtual human retina and a gene-regulatory analogue. The experiments reproduce non-identifiability under latent context, expose structure-mechanism confounding under latent edges, and recover pathway-level input-output relationships under targeted interventions, consistent with our positive Markov kernel identifiability results. Together, POSCMs provide an intervention-oriented framework for causal systems in which contexts, graph structure, mechanisms, and measurements are jointly generated and only partially observed.