human populations, as well as other model systems, is beginning to pinpoint numerous sites of nucleotide variation, that regardless of genomic loci, are capable of gene, alternative splicing, and downstream expression (Gerstein et al., 2010; Graveley et al., 2011; Lappalainen et al., 2013). However, linking any causal points of genetic inference with disease remains a significant challenge in the modern era for quantitative biology. Isolated studies often lack statistical power to definitively link any single SNP, let alone the interaction among multiple SNPs, with disease progression. Strategies are emerging to overcome these types of hurdles and identify unanticipated points of genetic interaction (Pan, 2008; Pandey et al., 2010). Similar to other complex traits, alcoholism is driven by the interaction of countless SNPs and competing environmental influences, which shape the transcriptome and regulate neurobiological functions. Although a number of differences may exist between human DNA and RNA sequences from the same individual (Li et al., 2011), sequencing the transcriptome in alcoholic brain tissue will continue to provide a valuable resource that represents the multidimensional factors operating in alcohol use disorders.
