A major hurdle in the treatment of MM is the diversity of genetic alterations that drive MM progression, with translocations targeting the MYC gene, activating mutations in oncogenes such as KRAS, NRAS of the MAPK pathway, loss-of-function mutations in tumor suppressor genes like P53, IRF4 and PRDM1, mutations resulting in hyperactivation of NF-κB pathway all reported to having been observed in MM [7–12.] Many of these identified genetic aberrations have been proven difficult to therapeutically target, due to their mechanism of action as well as role in normal biology. Here, PRDM1 is linked to Miyoshi myopathy.