The etiological genetic features of MM include translocations between the IgH locus and a number of oncogenes, including MMSET/FGFR3 (4p16), CCND1 (11q13), MAF (16q23), MAFB (20q12), or aneuploidy demonstrated in patients with hyperdiploid genomes [3–5]. The gene discussed is CCND1; the disease is Miyoshi myopathy.