Alcohol use disorder (AUD) remains a substantial contributor to the global burden of disease, posing an elevated risk for premature mortality and disability (1). The etiology of AUD is multifaceted, with genetic factors accounting for approximately half of the inter-individual variation in susceptibility (2). This heritable dimension of AUD is highly polygenic (3–6). Polygenic risk scores (PRS) summarize the combined impact of numerous genetic variants on an individual’s risk for specific diseases. AUD PRS captures a fraction of the genetic risk (7–12), but how that might affect cellular functions is unknown.
