Let G beacausalQ = Pr.

In this paper, we study the identification of nested counterfactuals from an arbitrary combination of observations and experiments. Specifically,building onamore explicit definition ofnested counterfactuals, we prove the counterfactual unnesting theorem (CUT), which allows one to map arbitrary nested counterfactuals to unnested ones.

A common approach for handling missing values in data analysis pipelines is multiple imputation via software packages such as MICE (Van Buuren and Groothuis-Oudshoorn, 2011) and Amelia (Honaker et al., 2011). These packages typically assume the data are missing at random (MAR), and impose parametric or smoothing assumptions upon the imputing distributions in a way that allows imputation to proceed even if not all missingness patterns have support in the data. Such assumptions are unrealistic in practice, and induce model misspecification bias on any analysis performed after such imputation. In this paper, we provide a principled alternative. Specifically, we develop a new characterization for the full data law in graphical models of missing data. This characterization is constructive, is easily adapted for the calculation of imputation distributions for both MAR and MNAR (missing not at random) mechanisms, and is able to handle lack of support for certain patterns of missingness. We use this characterization to develop a new imputation algorithm -- Multivariate Imputation via Supported Pattern Recursion (MISPR) -- which uses Gibbs sampling, by analogy with the Multivariate Imputation with Chained Equations (MICE) algorithm, but which is consistent under both MAR and MNAR settings, and is able to handle missing data patterns with no support without imposing additional assumptions beyond those already imposed by the missing data model itself. In simulations, we show MISPR obtains comparable results to MICE when data are MAR, and superior, less biased results when data are MNAR. Our characterization and imputation algorithm based on it are a step towards making principled missing data methods more practical in applied settings, where the data are likely both MNAR and sufficiently high dimensional to yield missing data patterns with no support at available sample sizes.

A key question in many network studies is whether the observed correlations between units are primarily due to contagion or latent confounding. Here, we study this question using a segregated graph (Shpitser, 2015) representation of these mechanisms, and examine how uncertainty about the true underlying mechanism impacts downstream computation of network causal effects, particularly under full interference -- settings where we only have a single realization of a network and each unit may depend on any other unit in the network. Under certain assumptions about asymptotic growth of the network, we derive likelihood ratio tests that can be used to identify whether different sets of variables -- confounders, treatments, and outcomes -- across units exhibit dependence due to contagion or latent confounding. We then propose network causal effect estimation strategies that provide unbiased and consistent estimates if the dependence mechanisms are either known or correctly inferred using our proposed tests. Together, the proposed methods allow network effect estimation in a wider range of full interference scenarios that have not been considered in prior work. We evaluate the effectiveness of our methods with synthetic data and the validity of our assumptions using real-world networks.

Estimating causal effects is crucial for decision-makers in many applications, but it is particularly challenging with observational network data due to peer interactions. Many algorithms have been proposed to estimate causal effects involving network data, particularly peer effects, but they often overlook the variety of peer effects. To address this issue, we propose a general setting which considers both peer direct effects and peer indirect effects, and the effect of an individual's own treatment, and provide identification conditions of these causal effects and proofs. To estimate these causal effects, we utilize attention mechanisms to distinguish the influences of different neighbors and explore high-order neighbor effects through multi-layer graph neural networks (GNNs). Additionally, to control the dependency between node features and representations, we incorporate the Hilbert-Schmidt Independence Criterion (HSIC) into the GNN, fully utilizing the structural information of the graph, to enhance the robustness and accuracy of the model. Extensive experiments on two semi-synthetic datasets confirm the effectiveness of our approach. Our theoretical findings have the potential to improve intervention strategies in networked systems, with applications in areas such as social networks and epidemiology.

It is often said that the fundamental problem of causal inference is a missing data problem -- the comparison of responses to two hypothetical treatment assignments is made difficult because for every experimental unit only one potential response is observed. In this paper, we consider the implications of the converse view: that missing data problems are a form of causal inference. We make explicit how the missing data problem of recovering the complete data law from the observed law can be viewed as identification of a joint distribution over counterfactual variables corresponding to values had we (possibly contrary to fact) been able to observe them. Drawing analogies with causal inference, we show how identification assumptions in missing data can be encoded in terms of graphical models defined over counterfactual and observed variables. We review recent results in missing data identification from this viewpoint. In doing so, we note interesting similarities and differences between missing data and causal identification theories.

Unobserved confounding is a fundamental obstacle to establishing valid causal conclusions from observational data. Two complementary types of approaches have been developed to address this obstacle. An extensive line of work (Wright, 1928; Angrist and Krueger, 2001; Kuroki and Pearl, 2014) is based on taking advantage of fortuitous external aids (such as the presence of an instrumental variable or other proxy), along with additional assumptions to ensure identification. A recent line of work of proximal causal inference (Miao et al., 2018a; Tchetgen Tchetgen et al., 2020) has aimed to provide a novel approach to using proxies to deal with unobserved confounding without relying on stringent parametric assumptions. On the other hand, a complete characterization of identifiability of a large class of causal parameters in arbitrary causal models with hidden variables has been developed using the language of graphical models, resulting in the ID algorithm and related extensions (Tian and Pearl, 2002; Shpitser and Pearl, 2006a,b; Huang and Valtorta, 2006; Shpitser and Sherman, 2018). Celebrated special cases of this approach, such as the frontdoor model (Pearl, 1995), are able to obtain non-parametric identification in seemingly counter-intuitive situations when a treatment and an outcome share an arbitrarily complicated unobserved common cause. In this paper we aim to develop a synthesis of the proximaland graphicalapproachesto identification in causal inference to yield the most general identification algorithm in multivariate systems currently known - the proximal ID algorithm. In addition to being able to obtain non-parametric identification in all cases where the ID algorithm succeeds, our approach allows us to systematically exploit proxies to adjust for the presence of unobserved confounders that would have otherwise prevented identification. In addition, we outline a class of estimation strategies for causal parameters identified by our method in an important special case.

In many applied fields, researchers are often interested in tailoring treatments to unit-level characteristics in order to optimize an outcome of interest. Methods for identifying and estimating treatment policies are the subject of the dynamic treatment regime literature. Separately, in many settings the assumption that data are independent and identically distributed does not hold due to inter-subject dependence. The phenomenon where a subject's outcome is dependent on his neighbor's exposure is known as interference. These areas intersect in myriad real-world settings. In this paper we consider the problem of identifying optimal treatment policies in the presence of interference. Using a general representation of interference, via Lauritzen-Wermuth-Freydenburg chain graphs (Lauritzen and Richardson, 2002), we formalize a variety of policy interventions under interference and extend existing identification theory (Tian, 2008; Sherman and Shpitser, 2018). Finally, we illustrate the efficacy of policy maximization under interference in a simulation study.

Recently there has been sustained interest in modifying prediction algorithms to satisfy fairness constraints. These constraints are typically complex nonlinear functionals of the observed data distribution. Focusing on the causal constraints proposed by Nabi and Shpitser (2018), we introduce new theoretical results and optimization techniques to make model training easier and more accurate. Specifically, we show how to reparameterize the observed data likelihood such that fairness constraints correspond directly to parameters that appear in the likelihood, transforming a complex constrained optimization objective into a simple optimization problem with box constraints. We also exploit methods from empirical likelihood theory in statistics to improve predictive performance, without requiring parametric models for high-dimensional feature vectors.