Among the LCL genes differentially expressed upon exposure to ethanol, 1043 were differentially expressed in brain in one or more of eleven post mortem gene expression studies, fifty-eight of which also differed between alcoholics and controls (Supplementary Table 1). Most GWAS findings are in the non-protein coding portion of the genome, and are thought to influence gene expression. Trait-associated SNPs are more likely to be expression quantitative trait loci (Nicolae et al., 2010). We therefore examined the overlap between genes whose expression in LCLs was altered by ethanol and genes reported in GWAS studies. 284 were identified by at least one GWAS (Supplementary Table 1, GWAS references therein), including 8 that also differed between alcoholics and controls (Supplementary Table 1 & 2). Among the 284 genes, twelve were reported by two GWAS, including two genes associated with glutamate uptake. SLC9A9 (cation proton antiporter 9) is associated with alcohol dependence (Kendler et al., 2011), alcohol dependence symptom count (Wang et al., 2012); it was also associated with smoking (Vink et al., 2009) and ADHD (Kondapalli et al., 2013). SLC9A9 expression was
