More than half of the 410 genes (244) were involved in 54 significant GOBPs. As expected, ethanol oxidation was among them and four genes (ADH1B, ADH1C, ADH4, and ADH5) were involved. Compromised executive functioning (i.e., neuroadaptation) is one of the major mechanisms contributing to AUD [50] and not surprisingly, several significant GOBPs related to synaptic systems (synaptic signaling, synapse organization, synaptic plasticity, startle response) were identified (46 genes). Although the role of the synaptic system in AUD is well-established [50], however, only nine genes (CSMD1, DCC, DRD3, EIF4E, ERC2, LINGO2, MAPT, NRXN2, and TENM2) were implicated in previous GWAS of AUD-related phenotypes. We also found significant GOBPs related to learning and memory (27 genes), consistent with previous findings that AUD and neurodegenerative diseases share some genetic liability [51]. Nervous system development-related GOBPs were significant (69 genes), and genes involved may 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
