OP is a chronic, progressive systemic skeletal disease characterized by a reduction in bone density and an increased susceptibility to fractures.[48] FST is believed to regulate muscle and bone mass by inhibiting activin and myostatin in bone cells.[49] Animal studies have shown that decreased levels of FST are associated with reductions in bone mineral density, bone volume, and the number and thickness of trabeculae in mice.[50] There are relatively few clinical studies examining the effects of FST on bone tissue, and the results across different populations have been contradictory. The gene discussed is MSTN; the disease is bone disorder.