Beyond initial recurrent abnormalities such as hyperdiploidy, loss of chromosome 13 and non-random translocations involving the 14q32 locus, secondary genetic events such as deletions (13q, 17p), somatic mutations in RAS oncogenes and BRAF, the deregulation of bcl-2 and c-myc proteins, loss of tumor suppressor gene product function and other abnormalities highly contribute to MM progression [22]. This evidence concerns the gene BCL2 and Miyoshi myopathy.