controls (Blednov et al., 2001; Hill et al., 2003), suggesting that GIRK2 may be mediating the reinforcing and/or aversive motivational aspects of ethanol action. In a GWAS in the COGA sample with a neurophysiological phenotype (ERO theta power to targets in an oddball task) we have reported genome wide significant associations of KCNJ6 SNPs (Kang et al., 2012); however, the association of these SNPs with alcoholism (or other addictions phenotypes) in COGA were not examined. On the other hand, using a candidate gene approach, Clarke et al. (2011) reported a significant association of a KCNJ6 polymorphism (rs2836016) with alcohol dependence, hazardous drinking and early life stress, and suggested that individuals consumed more alcohol to experience its rewarding effects possibly mediated by the role of GIRK2 in dopaminergic signaling. However, this SNP is located in a different region of the KCNJ6 gene compared to the SNP explored in the current study. Since GIRK2/3 channels are exclusively expressed in VTA dopaminergic neurons (Cruz et al., 2004), these channel properties may have important implications for addiction in general and AUD in particular (Arora et al., 2010; Kotecki, 2015). Taken together, these findings may lead to uncovering new therapeutic targets as well as drug
