Homozygous deletion of methylthioadenosine phosphorylase (MTAP), present in ~15% of tumors, leads to accumulation of methylthioadenosine and partial inhibition of protein arginine methyltransferase 5 (PRMT5), creating a synthetic-lethal vulnerability that sensitizes tumors to PRMT5-targeted therapies. Researchers from Beone Medicines Ltd. presented preclinical efficacy data of BGB-58067, an MTA-cooperative PRMT5 inhibitor, in models of tumors with MTAP-deficiency.