In the present study, we focused on integrating the genomic information to transcriptomic data to identify gene (genetic background) × environment (alcohol exposure) interactions in the etiology of alcohol use disorders. As mentioned in the discussion we identified that genes that have altered expression due to alcohol exposure interact with risk genes (GWAS) to increase an individual’s risk of becoming dependent on alcohol. So, to translate these findings in animals, one has to mimic expression of hub genes as well as the risk gene to alter the pathways associated with alcoholism. We are also reporting the direction of effect of the differential expression. That should provide information that can be used to see whether knock-down or overexpression of key genes alters risk for AUD phenotypes in models. Also, the replication of the modules in rodent models indicates which models might be useful to study the effects of dysregulation in these models.
