Indeed, different genetic abnormalities have been detected in MM and play a role in the pathogenesis of MM, including (i) translocation of chromosome 14 (t[14;16] and t[14;4]), (ii) MYC amplification, (iii) activation of NRAS and KRAS, (iv) mutations in FGFR3 and TP53, and (v) inactivation of cyclin-dependent kinase inhibitors CDKN2A and CDKN2C (4, 5). Here, CDKN2A is linked to Miyoshi myopathy.