More recently, genome-wide association studies (GWAS) have been used to explore the genetic basis of AUD (Hart & Kranzler 2015; Tawa, Hall & Lohoff 2016). The most robust and replicated risk alleles in European, African American, and Asian ancestry populations map to alcohol-metabolizing enzyme genes on chromosome 4q22–23 and 12q24: ADH1B (Gelernter et al. 2014; Xu et al. 2015; Clarke et al. 2017), ADH1C (Treutlein et al. 2009; Edenberg et al. 2010; Frank et al. 2012; Gelernter et al. 2014; Clarke et al. 2017), ADH5 (Clarke et al. 2017), ADH7 (Park et al. 2013) and ALDH2 (Takeuchi et al. 2011; Yang et al. 2013; Park et al. 2013; Quillen et al. 2014; Jorgenson et al. 2017). More recent GWAS that target alcohol consumption rather than AUD have identified novel genes including KLB, which influence both high alcohol consumption in humans (Schumann et al. 2016; Clarke et al. 2017; Jorgenson et al. 2017) and ethanol preference in mice (Schumann et al. 2016).
