and consortia efforts to examine cannabis involvement are underway, this is currently the largest peer-reviewed meta-analysis of cannabis GWAS studies to date. A more recent and larger meta-analysis (N: 184,765), including data from the ICC (N: 35,297), 23andme (N: 22,683), and the UK Biobank (N: 126,785), is now available from Pasman et al.9. The Pasman et al. study9 implicated CADM2 and NCAM1 and additional genetic risk loci for cannabis ever use, including ZNF704 (zinc finger protein 704), RABEP2 (Rabaptin, RAB GTPase Binding Effector Protein 2)/ATP2A1 (ATPase Sarcoplasmic/Endoplasmic Reticulum Ca2+ Transporting 1), and ALDH2 (Aldehyde Dehydrogenase 2 Family Member). While some genes mentioned above have been previously identified via genetic association studies with addiction related phenotypes (e.g., ALDH2 and alcohol use disorders (AUDs)10), the biological mechanisms linking these genetic variants to cannabis use/abuse are largely unknown. Evidence that there are both shared and non-shared genetic contributions to substance use and substance use disorders11 necessitates an examination of whether individual loci and polygenic risk for cannabis ever use predicts progression to cannabis use and problems (e.g., DSM-5 disorder criteria) in independent samples. In addition, evidence that genetic influences on other substance use and disorders are modified by the social environment12,13 suggests that
