In light of the recent findings suggesting an important role of NF-κB2 signaling in the pathogenesis of human MM [6,17], we characterized the mouse plasma cell tumors to determine to what extent they recapitulate human MM, which is characterized by a marked increase in the bone marrow plasma cell content (>10% of the total bone marrow cellularity), monoclonal proliferation of plasma cells as indicated by the production of M-protein in the serum, osteolytic bone lesions and/or osteoporosis, and other related organ damages [20]. The gene discussed is MYOM2; the disease is Miyoshi myopathy.