Given that MTA and SAM bind to the same site on PRMT5 with similar affinity (64), the accumulation of MTA can compete with SAM for binding to PRMT5, resulting in the partial inhibition of PRMT5 activity and leading to the sensitivity of tumor cells harboring the MTAP gene deletion to the inhibition of MAT2A and PRMT5. This evidence concerns the gene MTAP and neoplasm.