Variations in many genes influence the risk for AUD; however, aside from functional variants in two alcohol-metabolizing enzymes, alcohol dehydrogenase and aldehyde dehydrogenase, each individual variant has only a small effect [1, 3, 6, 7]. In addition to genetic differences, environmental factors, and interactions among the variants also affect AUD risk [1, 3, 6]. Genome-wide association studies (GWAS) identify regions in the genome that affect risk for complex diseases [8], but to date, only a few AUD-associated loci have been unambiguously identified [7]. Most identified regions contain many variants that are inherited together (linkage disequilibrium), and identifying the causal variant amongst all the associated ones is a major challenge.
