At least 34 GWAS analyses (largest N=112,117 [58]) have been reported for alcohol use disorder, related alcohol phenotypes, or alcohol biomarkers from studies focused on European [13, 18, 59–74, 58, 75, 76], European and African [77–83], or Asian [84–88] ancestries, or multiple ancestries combined [89]. Table 2 presents the genome-wide significant and replicable SNP associations for self-reported phenotypes in or near seven loci—serpin family C member 1 (SERPINC1), glucokinase regulator (GCKR,) shugoshin 1 (SGOL1), β-klotho (KLB), alcohol dehydrogenase (ADH) cluster, autism susceptibility candidate 2 (AUTS2), and aldehyde dehydrogenase 2 (ALDH2); an eighth locus—transferrin (TF)—was implicated for biomarkers of excessive alcohol intake but has not been associated with alcohol use disorder or related phenotypes. Emerging evidence suggests that the ADH gene cluster contains more than one independent association signal [58]. Other genome-wide significant loci have been reported, but independent replication has not been attained [13, 59, 60, 64, 68, 70, 73, 74, 58].
