oxytocin, which is known to play a role in neuropsychiatric disorders, including alcohol and drug addiction [72, 73]. Moreover, we found that Hsp70/HSPA6 was differentially expressed as a result of genetic variant-induced splicing changes in any of the three skipped exons in ELOVL7, LINC00665, and NSUN4. HSPA6 is a splicing factor found to be significantly upregulated upon alcohol intake in multiple brain regions, which suggests it may contribute to mis-splicing in the brain transcriptome [12]. Thus, although the functional roles of these genes in AUD have not been well studied, our findings provide evidence that they not only exhibit alcohol-induced effects, but may also contribute to the risk for AUD. The genes identified in our analysis that have not been described in earlier studies might also prove to be important for AUD risk.
