As shown in Fig. 8A and B, we confirmed in our model that MLN4924 significantly increases CRBN protein expression; in addition, MLN4924 downregulated both mRNA and protein levels of the transcription factor MEIS2 (Fig. 8C and D), previously identified as an endogenous cellular substrate of the E3-ubiquitin ligase complex CRL4-cereblon (CRL4CRBN) [56], and recently described by our group as a regulator of IMiDs activity in MM, given its ability to regulate the expression of IRF4 and IKZF3 [47]. The gene discussed is IRF4; the disease is Miyoshi myopathy.