The molecular landscape of MPM is characterized by high inter-patient and intra-tumor heterogeneity, comparably low somatic mutational burden, frequent loss-of-function of tumor suppressors (BAP1, NF2, CDKN2A, TP53, TSC1, etc.), and occasional gain-of-function of proto-oncogenes (PIK3CA, EGFR, KRAS, NRAS, HRAS, BRAF, etc.)[2,4,10,11,12,13,14,15,16,17]. This evidence concerns the gene CDKN2A and neoplasm.