In glioblastoma multiforme, MTAP loss leads to MTA accumulation, which partially inhibits PRMT5, making the cells reliant on residual PRMT5 activity for survival. Targeting this remaining PRMT5 with MTA-cooperative inhibitors induces synthetic lethality, representing a promising targeted approach for MTAP-deleted gliomas. Researchers from Ryvu Therapeutics SA reported the preclinical profile of RVU-305, a PRMT5 inhibitor, in MTAP-deleted cancer models.