Alcohol (i.e. ethanol) produces differential effects in multiple brain areas, including reward pathways involving the ventral tegmental area, nucleus accumbens, and prefrontal cortex (for review see Harrison et al., 2017). GWAS has the potential to reveal previously unknown genetic variants affected by ethanol or genes modulating those proteins. Multiple GWAS studies have been used to probe alcoholism risk, defining affected cohorts by a variety of criteria, including DSM criteria for alcohol dependence (Bierut et al. 2010; Dick et al. 2008; Edenberg et al. 2010; Kendler et al. 2011), online survey AUD identification test (AUDIT) (Sanchez-Roige et al., 2017), and reward-related theta oscillations (a highly heritable neuroelectric endophenotype) (Clarke et al., 2011, 2017; Kang et al., 2012). However, some SNPs fail to meet significance cutoffs after multiple test correction, because the heterogeneity and complexity of factors contributing to alcohol use disorder risk requires large sample sizes to parse out significant associations (e.g. Treutlein et al., 2009). Several consortia across the world are gathering expanded datasets from alcohol use disorder families, including Australian Twin Family Study of AUDs (OZALC) and Collaboration of
