TGF-β, a potent inhibitor of terminal OB differentiation and mineralization,[17], [18], [19] is produced by OBs and osteocytes, and abundantly deposited in bone matrices in a latent form.[20] It is released from bone matrices through bone resorption[21] and activated by acids and matrix metalloproteinases secreted from OCs.[22], [23], [24] Because osteoclastic bone resorption is enhanced in MM, TGF-β appears to be abundant and active in MM bone lesions, and may play an important role in bone formation impaired by MM. Here, TGFB1 is linked to Miyoshi myopathy.