(p < 10–8) and replicable SNPs were located in the following genes or non-coding RNAs (ncRNAs): ADH1B, ADH1C, ADH7, ALDH2, LOC100507053 (Frank et al., 2012; Gelernter et al., 2014; Park et al., 2013). Not surprisingly, the SNPs in the genes encoding the alcohol metabolizing enzymes are among the common variants with the largest effects on AUD risk. The associations found in the alcohol-metabolizing enzyme genes represent the most consistent overall finding for GWAS of alcohol dependence to date and these results replicate findings from candidate gene and linkage studies which have found similar associations with these enzymes (Edenberg and Foroud, 2013). However, these results were somewhat discouraging because it was widely predicted that the GWAS-era would revolutionize our understanding of the genetics of complex traits including alcohol dependence by uncovering many novel and unexpected common genetic variants for alcohol dependence that have eluded linkage and candidate gene association studies.
