Significant genetic associations of hundreds of markers with alcohol use disorder have been reported (Li et al., 2011; Manzardo, McGuire, & Butler, 2015) although it has been difficult to consistently replicate these associations across studies (Forero, Lopez-Leon, Shin, Park, & Kim, 2015). In general, genetic association studies of alcohol highlight the importance of genes related to (1) alcohol metabolism (ADH); (2) processing of alcohol intermediates (e.g., ADH1B, ADH1C, and ALDH2) (Cui et al., 2009; Macgregor et al., 2009) and (3) neurotransmission pathways thought to be involved with stimulus-reward processing in the brain including dopaminergic (e.g., DRD2, MAOA, COMT), serotonergic (HTR3A, HTR1B, HTR3B), GABAergic (GABRA1, GABRA2, GAD1, KCNJ9/GIRK3), and glutamtergic (GRIN2C) pathways. Some of these genes have demonstrated functional significance either in animal, human, or molecular genetic studies of SUD (Addolorato et al., 2006; Lobo & Nestler, 2011; Melroy-Greif et al., 2017; Thanos et al., 2001; Vanyukov et al., 2007). SUD is generally characterized as a signalling imbalance through striatal inhibitory D2-like dopamine receptors (DRD2) although this is not necessarily consistent across all drugs. With the execption of cannabinoids, human imaging
