Indeed, cancer cells infiltrating the bone site can disrupt the physiological bone turnover by increasing osteoclasts (OCs) maturation both indirectly, by stimulating osteoblasts (OBs) to highly produce the Receptor Activator of Nuclear Factor Kappa B Ligand (RANKL) and reduce osteoprotegerin (OPG) release, and directly by expressing RANKL and other OC modulating factors. Here, TNFRSF11B is linked to cancer.