Overexpression of the histone methyltransferase gene EZH2 commonly observed in MM is induced by dysregulated noncanonical NF-κB signaling; here, the inhibition of EZH2 sensitizes MM cells to proteasome inhibitors (PI, e.g., bortezomib), through MYC suppression and inhibition of H3K27 trimethylation, two critical regulators of genes involved in antibody production and B cell metabolism [19]. This evidence concerns the gene NFKB1 and Miyoshi myopathy.