First, variant‐level results for the reported alcohol consumption and AUD GWAS largely replicated previous findings (e.g., variation in ADH1B). 19 , 23 , 27 , 28 Results of additional gene‐level and neuroimaging genetic correlation analyses also corroborate results from prior studies. For AUD, gene‐based associations with the D2 dopamine receptor gene (DRD2) were observed along with dlPFC neuronal tissue‐specific enrichment of PDE4B, which encodes for an enzyme involved in dopamine signalling, highlighting regulatory effects on dopaminergic pathways recently linked to a broad genetic addiction liability factor. 57 Further, the association between AUD and variants related to decreased volume of the left pars orbitalis replicates recent Mendelian randomisation findings examining causal influences of brain morphology on problematic alcohol use. 58
