nearest genes within the same loci. Recent studies on psychiatric and neurological disorders showed that the most of genome-wide significant variants occur on active enhancers or promoters and might alter the expression level of nearby (cis) or distant (trans) gene[66–68]. These gene expression altering SNPs (expression quantitative loci or eQTLs) can be specific to a particular cell or tissue type. Several post-genomic helper tools such as FUMA[69] are available to functionally annotate the GWAS variants and to predict the functional consequence of a disease associated variant. More recent tools such as PrediXcan[70] and TWAS[71] can impute the genetic component of tissue-specific gene expression in GWAS datasets and help to connect changes in gene expression to trait outcome. Although size of eQTL and transcriptomic datasets can be a limiting factor to detect all functional association. Still initial application of PrediXcan has prioritized several genes (e.g. MAPT, CRHR1, FUT2, ADH1B, ADH4, ADH5, C1QTNF4, GCKR, DRD2) across different tissues [61, 72]. In a recent study some of these genetic targets including ADH1B, GCKR, SLC39A8 and KLB have been shown to play a conserved role in phenotypic responses to alcohol in Caenorhabditis elegans [74]. Researchers are also using the post-mortem brain tissue from alcoholic
