The Collaborative Study on the Genetics of Alcoholism (COGA) collected a diverse set of phenotypes, including electroencephalogram (EEG) parameters, in the search for genes and endophenotypes associated with AUD [6, 7]. A family-based, genome-wide association study (GWAS) of a frontal theta event-related oscillation (ERO) phenotype identified an association with several single nucleotide polymorphisms (SNPs), including a synonymous SNP, rs702859, in the KCNJ6 gene on chromosome 21 [8]. More recent studies concluded that this polymorphism influences the magnitude and topography of ERO theta power during reward processing in a monetary gambling task, reflecting a genetic link to neuronal circuits [9, 10]. Two other SNPs (rs702860 and rs2835872) within KCNJ6 were linked with the ERO endophenotype and AUD, but are noncoding, either intronic or within the 3′ untranslated region (3’ UTR), respectively. Additional studies identified various genetic loci correlating with selected EEG results but all consistently include alcohol dependence [11, 12]. To understand how these SNPs might influence these phenotypes, it is essential to characterize the pathways and mechanisms by which genetic risk unfolds at molecular, cellular and network resolutions. Furthermore, since
