In 2013, alcohol use disorder (AUD) affected >16.3 million people over the age of 18 (Murray and Lopez, 2013) and cost society nearly $250 billion in 2010 (Sacks et al., 2015). For the past 20+ years, evidence has been accumulating for a strong genetic component to AUD. Family and twin-based studies estimated a 45%-65% heritability (Heath et al., 1997; Kendler et al., 1994; Pickens et al., 1991), and a recent meta-analysis also estimated the heritability to be ~49% (Verhulst et al., 2015). In animal studies, selectively bred (Bell et al., 2012) and genetically engineered rodent models (Crabbe et al., 2006) of alcohol consumption also support a genetic component to AUD. In addition to genetics, environmental exposure also contributes to disease development and severity. For example, early life stress has been shown to play a significant role in AUD (Clarke et al., 2011). Heritability of neuropsychiatric disorders like AUD is notoriously complex and has been the subject of intense investigation (for reviews, see Geschwind and Flint, 2015; McConnell et al., 2017). Studying AUD from a genetic perspective is particularly challenging due
