These data indicate that BETi or selective degradation of BRD4 by specific PROTACs can modulate MEIS2 expression in human MM cells and suggest a possible cross-talk between MEIS2 and BET proteins in MM, where the repression of this transcription factor by this class of epigenetic drugs can enhance anticancer activity increasing apoptosis. The gene discussed is MEIS2; the disease is Miyoshi myopathy.