These data can explain the observed increase of MICA and PVR/CD155 expression and, at the same time, the antiproliferative/pro-apoptotic activity of reduced expression of MEIS2 in combination with different chemotherapics, both mediated by downregulation of IRF4 and MYC, important regulators of transcriptional networks involved in MM survival, drug-resistance and progression17,18,39–41. This evidence concerns the gene IRF4 and Miyoshi myopathy.