Estimating causal effects of joint interventions on multiple variables is crucial in many domains, but obtaining data from such simultaneous interventions can be challenging. Our study explores how to learn joint interventional effects using only observational data and single-variable interventions. We present an identifiability result for this problem, showing that for a class of nonlinear additive outcome mechanisms, joint effects can be inferred without access to joint interventional data. We propose a practical estimator that decomposes the causal effect into confounded and unconfounded contributions for each intervention variable. Experiments on synthetic data demonstrate that our method achieves performance comparable to models trained directly on joint interventional data, outperforming a purely observational estimator.

The goal of Root Cause Analysis (RCA) is to explain why an anomaly occurred by identifying where the fault originated. Several recent works model the anomalous event as resulting from a change in the causal mechanism at the root cause, i.e., as a soft intervention. RCA is then the task of identifying which causal mechanism changed. In real-world applications, one often has either few or only a single sample from the post-intervention distribution: a severe limitation for most methods, which assume one knows or can estimate the distribution. However, even those that do not are statistically ill-posed due to the need to probe regression models in regions of low probability density. In this paper, we propose simple, efficient methods to overcome both difficulties in the case where there is a single root cause and the causal graph is a polytree. When one knows the causal graph, we give guarantees for a traversal algorithm that requires only marginal anomaly scores and does not depend on specifying an arbitrary anomaly score cut-off. When one does not know the causal graph, we show that the heuristic of identifying root causes as the variables with the highest marginal anomaly scores is causally justified. To this end, we prove that anomalies with small scores are unlikely to cause those with larger scores in polytrees and give upper bounds for the likelihood of causal pathways with non-monotonic anomaly scores.

We study the differences arising from merging predictors in the causal and anticausal directions using the same data. In particular we study the asymmetries that arise in a simple model where we merge the predictors using one binary variable as target and two continuous variables as predictors. We use Causal Maximum Entropy (CMAXENT) as inductive bias to merge the predictors, however, we expect similar differences to hold also when we use other merging methods that take into account asymmetries between cause and effect. We show that if we observe all bivariate distributions, the CMAXENT solution reduces to a logistic regression in the causal direction and Linear Discriminant Analysis (LDA) in the anticausal direction. Furthermore, we study how the decision boundaries of these two solutions differ whenever we observe only some of the bivariate distributions implications for Out-Of-Variable (OOV) generalisation.

The investigation of the question "which treatment has a causal effect on a target variable?" is of particular relevance in a large number of scientific disciplines. This challenging task becomes even more difficult if not all treatment variables were or even can not be observed jointly with the target variable. In this paper, we discuss how causal knowledge can be obtained without having observed all variables jointly, but by merging the statistical information from different datasets. We show how the maximum entropy principle can be used to identify edges among random variables when assuming causal sufficiency and an extended version of faithfulness, and when only subsets of the variables have been observed jointly.