The abnormal activation of oncogenes such as CCND1, CCND2, CCND3, and FGFR3 has been reported in MM.[2, 4] DNA gains and losses that result in copy number alterations cause oncogene activation and tumor suppressor gene inactivation; these are the driving events leading to the development and progression of MM.[1, 2, 5] For example, the amplification of chromosome 1q, which harbors a number of potentially relevant oncogenes such as CKS1B,[6]ILF2,[7]ANP32E,[8] and PDZK1,[9] contributes to MM cell proliferation. This evidence concerns the gene ANP32E and Miyoshi myopathy.