MPM is currently considered a heterogeneous tumor with a variety of genomic and molecular alterations, including the loss of tumor suppressor genes such as CDKN2A/ARF (cyclin-dependent kinase inhibitor 2A/alternative reading frame), BAP1 (BRCA1 Associated Protein 1), and NF2 (neurofibromatosis type 2), single-nucleotide polymorphisms (SNPs) in genes involved in DNA repair mechanisms [6], and epigenetic and non-coding RNAs mutations [5,7]. This evidence concerns the gene CDKN2A and neoplasm.