Diverse genetic and environmental effects influence patterns of alcohol use in humans and animal models 60, 61, with 50-60% of the risk of alcoholism being a consequence of genetic factors 62, 63. Alcohol consumption measures are reliable and valid indices of alcohol usage in human reports 64, 65. Gene networks affiliated with lifetime alcohol consumption were enriched for genetic association signals involving alcohol dependence (Fig. 5), providing convergent evidence for an aggregate of genes as causal determinants in disease progression. Disease-specific sequence variant commonalities were modest, but may be due to localization of SNPs within non-coding regions of DNA 66. Sequencing of DNA and RNA isolated from the same subjects could provide even greater detail of the genetic architecture of transcriptional variation and subsequent behavioral traits. Prior studies on candidate genes, such as AUTS2, have demonstrated a potential role for intronic SNPs in alcohol consumption 67. Allelic variation within the intronic SNP rs6943555 of AUTS2 was also associated with altered mRNA expression in human prefrontal cortex 67. Transcriptome meta-analysis of mice differing in voluntary alcohol consumption also showed expression differences
