AD and AUD are complex disorders in which both genetic differences and environmental factors affect the risk (Walters et al., 2018, Edenberg and Foroud, 2013, Edenberg and McClintick, 2018, Hart and Kranzler, 2015, Rietschel and Treutlein, 2013). Understanding the genetic differences associated with the risk of AD and AUD will provide insights into the biological mechanisms underlying the disease. They are heterogeneous disorders, and variations in many genes influence the risk. Individual variants make only small contributions to the risk (Edenberg and Foroud, 2013, Gelernter et al., 2014, Gelernter et al., 2019, Walters et al., 2018, Zhou et al., 2019), with the exception of the functional variants in two of the alcohol-metabolizing enzymes (ADH1B and ALDH2) (Edenberg and McClintick, 2018). Thus, identification of genetic variations that impact the risk of AD/AUD is challenging. With the idea that the heterogeneity may well reflect a range of genetic contributions to individual criteria and related traits, Genome Wide Association Studies (GWAS) have been carried out on AD and on individual criteria and related phenotypes. These have identified multiple loci (Walters et al., 2018,
