We introduce the best order score search (BOSS) and grow-shrink trees (GSTs) for learning directed acyclic graphs (DAGs) in this paradigm.

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We introduce the best order score search (BOSS) and grow-shrink trees (GSTs) for learning directed acyclic graphs (DAGs) in this paradigm.

LiNGAM determines the variable order from cause to effect using additive noise models, but it faces challenges with confounding. Previous methods maintained LiNGAM's fundamental structure while trying to identify and address variables affected by confounding. As a result, these methods required significant computational resources regardless of the presence of confounding, and they did not ensure the detection of all confounding types. In contrast, this paper enhances LiNGAM by introducing LiNGAM-MMI, a method that quantifies the magnitude of confounding using KL divergence and arranges the variables to minimize its impact. This method efficiently achieves a globally optimal variable order through the shortest path problem formulation. LiNGAM-MMI processes data as efficiently as traditional LiNGAM in scenarios without confounding while effectively addressing confounding situations. Our experimental results suggest that LiNGAM-MMI more accurately determines the correct variable order, both in the presence and absence of confounding.

In causal discovery, non-Gaussianity has been used to characterize the complete configuration of a Linear Non-Gaussian Acyclic Model (LiNGAM), encompassing both the causal ordering of variables and their respective connection strengths. However, LiNGAM can only deal with the finite-dimensional case. To expand this concept, we extend the notion of variables to encompass vectors and even functions, leading to the Functional Linear Non-Gaussian Acyclic Model (Func-LiNGAM). Our motivation stems from the desire to identify causal relationships in brain-effective connectivity tasks involving, for example, fMRI and EEG datasets. We demonstrate why the original LiNGAM fails to handle these inherently infinite-dimensional datasets and explain the availability of functional data analysis from both empirical and theoretical perspectives. We establish theoretical guarantees of the identifiability of the causal relationship among non-Gaussian random vectors and even random functions in infinite-dimensional Hilbert spaces. To address the issue of sparsity in discrete time points within intrinsic infinite-dimensional functional data, we propose optimizing the coordinates of the vectors using functional principal component analysis. Experimental results on synthetic data verify the ability of the proposed framework to identify causal relationships among multivariate functions using the observed samples. For real data, we focus on analyzing the brain connectivity patterns derived from fMRI data.

We consider the task of identifying the causal parents of a target variable among a set of candidate variables from observational data. Our main assumption is that the candidate variables are observed in different environments which may, for example, correspond to different settings of a machine or different time intervals in a dynamical process. Under certain assumptions different environments can be regarded as interventions on the observed system. We assume a linear relationship between target and covariates, which can be different in each environment with the only restriction that the causal structure is invariant across environments. This is an extension of the ICP ($\textbf{I}$nvariant $\textbf{C}$ausal $\textbf{P}$rediction) principle by Peters et al. [2016], who assumed a fixed linear relationship across all environments. Within our proposed setting we provide sufficient conditions for identifiability of the causal parents and introduce a practical method called LoLICaP ($\textbf{Lo}$cally $\textbf{L}$inear $\textbf{I}$nvariant $\textbf{Ca}$usal $\textbf{P}$rediction), which is based on a hypothesis test for parent identification using a ratio of minimum and maximum statistics. We then show in a simplified setting that the statistical power of LoLICaP converges exponentially fast in the sample size, and finally we analyze the behavior of LoLICaP experimentally in more general settings.

Complex diseases are caused by a multitude of factors that may differ between patients even within the same diagnostic category. A few underlying root causes may nevertheless initiate the development of disease within each patient. We therefore focus on identifying patient-specific root causes of disease, which we equate to the sample-specific predictivity of the exogenous error terms in a structural equation model. We generalize from the linear setting to the heteroscedastic noise model where $Y = m(X) + \varepsilon\sigma(X)$ with non-linear functions $m(X)$ and $\sigma(X)$ representing the conditional mean and mean absolute deviation, respectively. This model preserves identifiability but introduces non-trivial challenges that require a customized algorithm called Generalized Root Causal Inference (GRCI) to extract the error terms correctly. GRCI recovers patient-specific root causes more accurately than existing alternatives.

Causal discovery, the learning of causality in a data mining scenario, has been of strong scientific and theoretical interest as a starting point to identify "what causes what?" Contingent on assumptions, it is sometimes possible to identify an exact causal Directed Acyclic Graph (DAG), as opposed to a Markov equivalence class of graphs that gives ambiguity of causal directions. The focus of this paper is on one such case: a linear structural equation model with non-Gaussian noise, a model known as the Linear Non-Gaussian Acyclic Model (LiNGAM). Given a specified parametric noise model, we develop a novel sequential approach to estimate the causal ordering of a DAG. At each step of the procedure, only simple likelihood ratio scores are calculated on regression residuals to decide the next node to append to the current partial ordering. Under mild assumptions, the population version of our procedure provably identifies a true ordering of the underlying causal DAG. We provide extensive numerical evidence to demonstrate that our sequential procedure is scalable to cases with possibly thousands of nodes and works well for high-dimensional data. We also conduct an application to a single-cell gene expression dataset to demonstrate our estimation procedure.