Alcohol use and alcohol use disorder (AUD) are leading causes of death and disability worldwide [1]. Genome-wide association studies (GWAS) of AUD and problematic drinking measured by different assessments have identified potential risk genes primarily in European populations [2–5]. Quantity-frequency measures of drinking, for example the Alcohol Use Disorders Identification Test–Consumption (AUDIT-C), which sometimes reflect alcohol consumption in the normal range, differ genetically from AUD and measures of problematic drinking (e.g., the Alcohol Use Disorders Identification Test–Problems [AUDIT-P]), and show a divergent set of genetic correlations [3, 4]. The estimated SNP-based heritability (h2) of AUD ranges from 5.6% to 10.0% [2–5]. To date, more than 10 risk variants have been significantly associated with AUD and AUDIT-P (p < 5 × 10−8). Variants that have been mapped to several risk genes in multiple studies include ADH1B (Alcohol Dehydrogenase 1B (class I), Beta Polypeptide), ADH1C (Alcohol Dehydrogenase 1C (class I), Gamma Polypeptide), ALDH2 (Aldehyde Dehydrogenase 2 Family Member, only in some Asian samples), SLC39A8 (Solute Carrier Family 39 Member 8), GCKR (Glucokinase Regulator), and CRHR1 (Corticotropin Releasing Hormone Receptor 1). In the
