While early chromosomal abnormalities, such as immunoglobulin heavy chain translocations or trisomies, are present in both MGUS and MM, secondary translocations or mutations involving oncogenes (e.g., MMSET, MYC, MAFB, IRF4, FGFR3, RAS family members, among many others) (11) or tumor suppressors (e.g., CDKN2A, CDKN2C, or TP53) are unique to MM and absent in MGUS (12). This evidence concerns the gene TP53 and Miyoshi myopathy.