Since activation of NF-κB pathways, especially the non-canonical NF-κB pathway, has been frequently observed in MM [41], and the RelB-p52 addiction has been found in most subgroups of MM cells [42], the RelB-mediated NF-κB pathway activation by G9a upregulation may serve as an important epigenetic mechanism of MM proliferation and survival, which makes the G9a an important molecular target for NF-κB pathway inhibitors and innovative therapeutic approaches for MM patients. This evidence concerns the gene NFKB1 and Miyoshi myopathy.