Group1 of the upper quartile was the least variable contingent of modules, with the greatest inter-module correlation among 1030 genes (Fig. S6), promoting the observed differences in disease status and excessive alcohol consumption. Functional enrichment of elements contained within Group1 largely accounted for gene ontologies corresponding to lifetime alcohol consumption within the upper quartile (Fig. 2e). This set of transcripts within Group1 are preserved for neuronal protein-protein coexpression (P = 1.19 e-36) 44, suggesting the GMs may extend beyond co-regulated RNA transcripts. Additionally, this network substructure is further over-represented for a meta-analysis of alcohol drinking behavior in mice (P = 4.59 e-08) 45, providing independent evidence for a cohesive group of genes involved in alcohol consumption. Despite the fact our analysis has focused on molecular networks for lifetime alcohol consumption, a portion of these jointly expressed genes may be indirectly regulated by common substrates and closely associated endophenotypes governing the pathophysiology of alcohol dependence. MicroRNA miR-9, a post-transcriptional regulator of splice variation and neuroadaptations of alcohol tolerance (a hallmark of escalated alcohol drinking), targets a notable share of genes within
