Among the most common genetic alterations or deregulated pathways identified in MM, deletions in the cyclin‐dependent kinase inhibitor 2A (CDKN2A) locus, inactivation of the retinoblastoma (RB) pathway, mutations in the BRCA1‐associated protein 1 (BAP1) and neurofibromatosis type 2 (NF2) genes, and aberrant regulation of phosphatidylinositol‐4,5‐ bisphosphate 3‐kinase (PI3K)/AKT pathway are all related to MM uncontrolled growth and resistance to treatment‐induced cell death.10, 11, 12. This evidence concerns the gene BAP1 and Miyoshi myopathy.