Although the number of genetic variations identified has increased rapidly, the understanding of how genetic variations contribute to disease susceptibility has lagged behind. Earlier studies mainly focused on nonsynonymous SNPs [9,10]. More recent studies have attempted to explain functional mechanisms of action of haplotypes that contain SNP and other regulatory variants [11-17]. A number of haplotypes defined by specific SNPs have been found to alter gene expression by modifying transcription factor binding sites [11], microRNA binding sites [12-15] and alternative splicing [16]. Others regulate signaling pathways [17]. However to date there have been only modest genome-scale efforts to study the molecular mechanisms of addiction-associated genetic variants. The relative contributions of different molecular mechanisms remain largely unknown.
