PRMT5 and neoplasm: In addition, the frequent deletion of methylthioadenosine phosphorylase (MTAP) as a consequence of 9p21 loss in cancer cells leads to the dysregulation of methionine metabolism and makes tumor cells more sensitive to protein arginine N-methyltransferase 5 (PRMT5) inhibitors, creating a new therapeutic opportunity based on methionine metabolism and epigenomic interactions (Kryukov et al., 2016; Marjon et al., 2016; Mavrakis et al., 2016).