The upregulation of RANKL induces the activation and growth of osteoclasts through the osteoprotegerin-RANK pathway, thereby promoting the osteoclastic activity of the cancer cells.[87] Concurrently, these osteoclasts resorb bone and secrete growth factors such as BMPs, IGFs, and FGFs, which further stimulate the proliferation of metastatic cancer cells[88] (Fig. 3). The gene discussed is TNFSF11; the disease is cancer.