The deregulation of B and plasma cell transcription factors mediated by PRC2 targeting and IMiDs results in a significant shift between proliferation and quiescence with a significant increase in the percentage of ki67 negative MM cells and a significant induction of quiescent cell features including repression of E2F1 and higher level of p21 Cdk inhibitor [67–70]. The gene discussed is CDKN1A; the disease is Miyoshi myopathy.