On the contrary, lentiviral-mediated transient overexpression of MEIS2 in SKO-007(J3) cells abrogated upregulation of MICA and PVR/CD155 in Lenalidomide treated cells (Fig. 5a–e), in agreement with the hypothesis of MEIS2 as a functional intracellular competitor of IMiDs activity in MM. This evidence concerns the gene MEIS2 and Miyoshi myopathy.