Partially Observed Structural Causal Models

arXiv cs.LG / 5/6/2026

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Key Points

  • The paper introduces Partially Observed Structural Causal Models (POSCMs), extending structural causal models to settings where latent contexts jointly determine both interaction structure and downstream mechanisms on observed variables.
  • POSCMs support an intervention hierarchy that includes both node-level and edge-level context/variable interventions, enabling more “surgical” causal edits than standard SCMs.
  • The authors use a Kolmogorov-Arnold-Sprecher (KAS) edge-functional decomposition to explicitly parametrize dyadic functional contributions and to represent each node mechanism as a sum of univariate functions of its parents.
  • A new identifiability theory specifies which families of interventions are sufficient to separate structure formation effects from mechanism effects, addressing ambiguity that arises when key contexts are latent.
  • Empirical validation in a virtual human retina simulator shows (a) predicted non-identifiability when context is fully latent, (b) structure–mechanism confounding when only node interventions are available with latent edges, and (c) recovery of synaptic input–output relationships using targeted node interventions aligned with the proposed positive identifiability result.

Abstract

Here we introduce Partially Observed Structural Causal Models (POSCMs) that formalize causal systems where latent contexts co-determine both the interaction structure and downstream mechanisms on observed variables. POSCMs provide an extension of structural causal models (SCMs), as a self-contained causal modeling framework for endogenous graphs, allowing for an intervention hierarchy spanning node- and edge-level context and endogenous variable interventions. To enable surgical edge interventions, we adopt a Kolmogorov-Arnold-Sprecher edge-functional decomposition, an existence theorem for representing each node mechanism as a sum of univariate functions of its parents, yielding an explicit parametrization of dyadic functional contributions. We provide an identifiability theory that clarifies which intervention families would suffice to disentangle structure formation from mechanisms. We empirically validate these predictions in a biophysically detailed virtual human retina simulator, constructing intervention protocols that (i) reproduce the non-identifiability predicted when context is latent and no context-level interventions are available, (ii) exhibit structure-mechanism confounding under latent edges when only node interventions are observed, and (iii) recover synaptic input-output relationships via targeted node interventions, consistent with our positive kernel identifiability result. Our work generalizes SCMs in a way that allows it to work in a world closer to the one we live in.