Accordingly, to Mavrakis et al. (2016) [22] and Marjon K et al. (2016) [23] deletions at 9p abrogating the MTAP gene lead to the accumulation of its substrate 5′ methilthioadenosine (MTA) and a metabolic “rewiring” of the tumor cells, which rendered them specifically sensible to drugs that inhibit the methyltransferase axis composed by: Methionine Adenosyltransferase II alpha (MAT2A), Protein Arginine Methyltransferase 5 (PMRT5) and Rio domain containing protein 1 (RIOK1). The gene discussed is PRMT5; the disease is neoplasm.