However, other genes are consistently dysregulated specifically in the transition to MM, but not in Eμ-xbp-1s B cells or in the nontransgenic B cells such as BAFF, APRIL, and several genes associated in MM human studies with a high degree of proliferation and poor prognosis (TOP2A, BIRC5, CCNB2, NEK2, AURKA, BUB1, CDC2, and CDCA1; data not shown), suggesting that other genetic and/or epigenetic additional lesions are needed to drive the progression into MGUS and furthermore into MM. Here, TOP2A is linked to Miyoshi myopathy.