A ProbLog program is a logic program with facts that only hold with a specified probability. In this contribution, we extend this ProbLog language by the ability to answer “What if” queries. Intuitively, a ProbLog program defines a distribution by solving a system of equations in terms of mutually independent predefined Boolean random variables. In the theory of causality, Judea Pearl proposes a counterfactual reasoning for such systems of equations. Based on Pearl’s calculus, we provide a procedure for processing these counterfactual queries on ProbLog programs, together with a proof of correctness and a full implementation. Using the latter, we provide insights into the influence of different parameters on the scalability of inference. Finally, we also show that our approach is consistent with CP-logic, that is with the causal semantics for logic programs with annotated with disjunctions.

Given the complexity of cyber-physical systems (CPS), such as swarms of drones, often deviations, from a planned mission or protocol, occur which may in some cases lead to harm and losses. To increase the robustness of such systems, it is necessary to detect when deviations happen and diagnose the cause(s) for a deviation. We build on our previous work on soft agents, a formal framework based on using rewriting logic for specifying and reasoning about distributed CPS, to develop methods for diagnosis of CPS at design time. We accomplish this by (1) extending the soft agents framework with Fault Models; (2) proposing a protocol specification language and the definition of protocol deviations; and (3) development of workflows/algorithms for detection and diagnosis of protocol deviations. Our approach is partially inspired by existing work using counterfactual reasoning for fault ascription. We demonstrate our machinery with a collection of experiments.

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects.