To conclude, although exogenous myostatin limits osteoblast differentiation, yet stimulates osteoclast maturation in vivo (Figure 2; Table 1); and although the inhibition of myostatin improves muscle and bone properties in murine models of diseases including OI, osteoporosis, and diabetes, the benefits of myostatin therapeutics in human musculoskeletal disorders still need to be validated. This evidence concerns the gene MSTN and diabetes mellitus.