We had already shown in a previous paper that IMiDs have the ability to upregulate the expression of NK cell-activating ligands in MM cells, a pathway involving a mechanism of derepression of MICA and PVR/CD155 genes by IMiDCRBN-mediated degradation of IKZF1/3 and inhibition of IRF4 expression46. The gene discussed is MICA; the disease is Miyoshi myopathy.