predispose to AUD via mechanisms yet to be discovered. GOBPs such as protein metabolic process, cell adhesion, cell development, cell junction organization, movement of cell or subcellular component, cell-cell signaling, and regulation of signaling were also significant. Intuitively, these GOBPs may not seem to be AUD-related, however, among 148 genes only involved in these processes, 20 of them were reported in previous GWAS of AUD-related phenotypes with some of them, e.g., FTO, PDE4B, and SLC39A8, being genome-wide significant in recent large-scale GWAS of AUD [7]. In addition, there were seven genes (EHBP1, EYS, FNBP4, LOC100507053, TNRC6A, WDR7, and ZNF462) that were not involved in any significant GOBPs but were reported by previous GWAS of AUD-related phenotypes. Further studies are needed to elucidate the roles of these genes in predisposing to AUD. Tissue-specific enrichment showed that most genes were enriched in brain tissues as expected, however, other tissues such as liver, kidney, and pancreas also showed enrichment. Except liver, how these tissues relate to AUD remain to be discovered. By searching the drug target gene database, we found four genes (DRD2, PDE4B, GRM5, and SLC6A9) were already targets of AUD treatment drugs (Table S6). We also found 22 genes that were
