Alcohol Use Disorder (AUD) is a major contributor to the global disease burden, with a prevalence of ~17% among 12-month alcohol users in the US [1, 2] and an estimated heritability of 49% [3]. Knowledge about the molecular mechanisms can foster understanding of causes and promote prevention. Recent genome-wide association studies (GWASs) have identified 29 genetic loci associated with Problematic Alcohol Use (PAU), a proxy of AUD [4]. While GWASs identify increasing numbers of disease-associated loci, the functional interpretation of many of these findings remains inconclusive. Analyzing the transcriptome can extend the understanding of the molecular mechanisms underlying AUD, by identifying associated gene expression patterns. Findings can in turn be integrated with results from GWASs and epigenome-wide association studies (EWASs) to identify the pathomechanisms underlying disease.
