this is still ~ 2% of the total individual differences in AUD and may include non-splicing related DNA variants. The GWASs used in our study included some overlapping participants (e.g., UK BioBank and Million Veterans Project) and were limited to individuals of European Ancestry. Human brain data had long post-mortem intervals, which could lead to poor RNA quality and high RNA degradation—potentially biasing results towards shorter transcripts. Primate brain samples were not perfectly matched to the human data, as primates were limited to males, neuroanatomical location diverged (especially in PFC), and often the specific splicing events within genes differed across species. Lastly, the results from our study were based on computational analyses and require experimental follow-up to buttress the confidence of these findings and their role in AUD. Notwithstanding these limitations, our study added context to our genetic and neurobiological understanding of AUD.