Using integrated genomics on newly diagnosed patients with MM, Walker et al. [15], for example, identified 63 driver genes, including the most diverse oncogenes, such as FGFR3, DIS3, PRKD2, CCND1, IRF4, MAF, BRAF, DIS3, ATM, FAM46C and MYC. Among the most relevant secondary events, deregulated MYC activity is associated with disease progression[10] and occurs in a large percentage (67%) of MM case[16]. This evidence concerns the gene CCND1 and Miyoshi myopathy.