range of situations, including alcohol metabolism, human behavior, liver function, and human evolution [Brooks and Zakhari 2014; Buhler and others 2015; Carr and others 2002; Edenberg 2000; Edenberg 2007; Li and others 2011a; Li and others 2011b]. In recent years, omic studies based on high-throughput technologies confirmed the key role of ADH in multiple molecular mechanisms [Gelernter and others 2014; Kropotova and others 2014; Winnier and others 2015]. In particular, variation in the ADH1B gene was demonstrated to have a large effect in the predisposition to several complex traits, including alcoholism and (primarily GI tract) cancer [Gelernter and others 2014; McKay and others 2011; Wu and others 2012]. The relevance of the ADH1B locus was further confirmed by genomic analyses that highlighted how its genetic variation was shaped by selective pressures during human evolution [Galinsky and others 2016]. Due to its clear involvement in the major alcohol metabolic pathway, different authors have hypothesized that ADH1B phenotypic associations are related to alcohol use and its downstream consequences [Holmes and others 2014; Silverwood and others 2014]. However, recent findings have shown that ADH1B may affect the human phenome through alcohol-independent mechanisms also [Polimanti and others 2016a]. To understand the network of ADH1B
