In fact, the most prominent SNPs that have been linked to alcohol abuse, identified using genome wide association studies (GWAS), have been mapped to genes encoding liver enzymes, specifically alcohol dehydrogenase and aldehyde dehydrogenase (Tawa, Hall, & Lohoff, 2016). However, there are also a number of studies implicating genes that modulate synaptic function such as OPRM1, CHRNA5 and GABRA2 to alcohol abuse as well, suggesting that AUDs have a key neuropsychiatric component that has not been thoroughly investigated (Berrettini, 2013; Hoehe et al., 2000; D. Li et al., 2014; Lubke, Stephens, Lessem, Hewitt, & Ehringer, 2012). Moreover, it is more likely that a given individual with an AUD carries SNPs located in several genes, or even in non-coding regions, where each individual variant exerts a small effect on AUD risk but the additive sum of these variants together yields a significant impact (Mayfield, Harris, & Schuckit, 2008). It is also plausible that effects seen from specific SNPs vary from patient to patient due to each individual’s unique genetic background. This suggests that the risk factors for the development of an
