In recent years, new treatment options have been developed, such as the monoclonal antibody denosumab directed against RANKL; denosumab does not affect the GCTB recurrence rate because it mainly affects the bone destructive osteoclast-like giant cells within the tumor, rather than the stromal cells.7, 23, 24 Here we used a series of in vitro and in vivo experiments to demonstrate that aberrantly increased expression of miR-125a stimulates stromal cell growth and tumorigenicity. The gene discussed is TNFSF11; the disease is neoplasm.