Estimating counterfactual distributions under interventions is central to treatment risk assessment and counterfactual generation tasks. Existing approaches model the counterfactual distribution as a standalone generative target, without exploiting its relationship to the observational data. In this work, we show that under standard assumptions, observational and counterfactual outcome distributions are tightly linked: they have identical support and tail behavior, remain statistically close under weak confounding, and share any features of high-dimensional outcomes which are invariant to confounders. These properties motivate learning counterfactual distributions not from scratch, but via a deconfounding flow from the observational distribution. We formulate this problem via flow-matching and derive a semiparametrically efficient estimator based on a novel efficient influence function correction. We subsequently extend our estimator to target minimal-energy flows in high-dimensions, which we show can be especially simple targets between observational and counterfactual distributions. In experiments, deconfounding flows outperform existing debiased counterfactual distribution estimators, while also mitigating known failure modes of flow-based methods.

Thm. 3.2] we can construct an SCM

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

A complete understanding of heterogeneous treatment effects involves characterizing the full conditional distribution of potential outcomes. To this end, we propose the Conditional Counterfactual Mean Embeddings (CCME), a framework that embeds conditional distributions of counterfactual outcomes into a reproducing kernel Hilbert space (RKHS). Under this framework, we develop a two-stage meta-estimator for CCME that accommodates any RKHS-valued regression in each stage. Based on this meta-estimator, we develop three practical CCME estimators: (1) Ridge Regression estimator, (2) Deep Feature estimator that parameterizes the feature map by a neural network, and (3) Neural-Kernel estimator that performs RKHS-valued regression, with the coefficients parameterized by a neural network. We provide finite-sample convergence rates for all estimators, establishing that they possess the double robustness property. Our experiments demonstrate that our estimators accurately recover distributional features including multimodal structure of conditional counterfactual distributions.

Importantly, our results also show that subpopulation-based recourse is the right approach to adopt when assumptions such as additive noise do not hold.

Counterfactual reasoning aims at answering contrary-to-fact questions like "Would have Alice recovered had she taken aspirin?" and corresponds to the most fine-grained layer of causation. Critically, while many counterfactual statements cannot be falsified--even by randomized experiments--they underpin fundamental concepts like individual-wise fairness. Therefore, providing models to formalize and implement counterfactual beliefs remains a fundamental scientific problem. In the Markovian setting of Pearl's causal framework, we propose an alternative approach to structural causal models to represent counterfactuals compatible with a given causal graphical model. More precisely, we introduce counterfactual models, also called canonical representations of structural causal models. They enable analysts to choose a counterfactual assumption via random-process probability distributions with preassigned marginals and characterize the counterfactual equivalence class of structural causal models. Using these representations, we present a normalization procedure to disentangle the (arbitrary and unfalsifiable) counterfactual choice from the (typically testable) interventional constraints. In contrast to structural causal models, this allows to implement many counterfactual assumptions while preserving interventional knowledge, and does not require any estimation step at the individual-counterfactual layer: only to make a choice. Finally, we illustrate the specific role of counterfactuals in causality and the benefits of our approach on theoretical and numerical examples.

Predicting counterfactual distributions in complex dynamical systems is essential for scientific modeling and decision-making in domains such as public health and medicine. However, existing methods often rely on point estimates or purely data-driven models, which tend to falter under data scarcity. We propose a time series diffusion-based framework that incorporates guidance from imperfect expert models by extracting high-level signals to serve as structured priors for generative modeling. Our method, ODE-Diff, bridges mechanistic and data-driven approaches, enabling more reliable and interpretable causal inference. We evaluate ODE-Diff across semi-synthetic COVID-19 simulations, synthetic pharmacological dynamics, and real-world case studies, demonstrating that it consistently outperforms strong baselines in both point prediction and distributional accuracy.

Pearl [2009] presents a "ladder of causation" that distinguishes three levels of causal concepts: associational (level 1), interventional (level 2), and counterfactual (level 3).