Some recent studies have proposed that certain subsets of MM are sensitive to EZH2 inhibition such as MM cases harboring recurring UTX/KDM6A loss-of-function mutations or recurring t(4:14) translocation, both of which are known to directly impact modification EZH2’s target residue and alter EZH2 distribution respectively [34]. This evidence concerns the gene KDM6A and Miyoshi myopathy.