copy number variations represent part of the risk architecture for OCD9. These findings emphasize the need for a comprehensive exploration of the contribution of both common and rare genetic factors, as well as their interplay, to OCD risk. Finally, with the implication of the MHC complex, we provide additional evidence for potential shared genetic influences underlying both OCD and increased liability to autoimmune processes, although the directionality of those relationships remains to be definitively elucidated. In addition to continuing to increase sample sizes, future studies will require ancestrally diverse samples to further facilitate the discovery of additional OCD risk variants. Similarly, sex-specific analyses and additional clinical phenotyping will allow for the further elucidation of genetic and clinical relationships between OCD and co-occurring disorders. Finally, with the emergence of drug databases describing the relations between drugs and molecular phenotypes89, our results may be useful for drug repurposing (i.e., identifying existing drugs targeting OCD risk genes), leading to new opportunities to find more effective treatments.
