Resulting structural alterations implicate two targets with critical impacts: recurrent TGFBR2 inactivation that promotes EBV persistence in tumor cells and MTAP deletion (adjacent to the CDKN2A/CDKN2B loci) with marked sensitivity to MAT2A inhibition potentially applicable to a broad subset of NPC patients. This evidence concerns the gene MAT2A and nasopharyngeal carcinoma.