As revealed by aCGH, structural rearrangements on SN-MM cell lines targeted a wide number of chromosome regions, including 1q, 5p, 6p, 6q, 8q and 9p, with a common consequence being gain of oncogenes, such as TERT, MYC, KRAS, or loss of tumor suppressor genes, such as ARID1B and CDKN2A. The loss of p16INK4a protein expression further support these data, suggesting that MM might benefit from therapeutic strategies targeting CDKN2A loss, including the pharmacological inhibition of CDK4/6 (i.e. palbociclib and ribociclib) that are targets of p16 INK4a [87]. This evidence concerns the gene KRAS and Miyoshi myopathy.