In fact, co-culture of monocytes with stromal cells including osteoblasts, fibroblasts, and cancer cells revealed that hypoxia-induced HIF-1α stimulates local production of pro-osteoclastogenic cytokines including receptor activator of nuclear factor kappa B ligand (RANKL), vascular endothelial growth factor (VEGF), inhibiting at the same time the production of osteoprotegerin (OPG), a soluble decoy receptor for RANKL that prevents osteoclasts maturation and activation [16, 17]. The gene discussed is VEGFA; the disease is cancer.