The gene encoding methylthioadenosine phosphorylase (MTAP) is expressed in normal tissues but 10 to 15% of tumors present deletions of MTAP expression that lead to accumulation of its metabolite 5-methylthioadenosine (MTA). Previous research has shown that selective inhibition of protein arginine methyltransferase 5 (PRMT5) in the presence of MTA may be considered a potential therapeutic strategy for the treatment of MTAP-deleted cancer.