TNFSF11 and neoplasm: Although agents targeting osteoclast activity, such as bisphosphonates and receptor activator of nuclear factor-κ B ligand (RANKL) inhibitors, have improved clinical management, they do not fully interrupt the “vicious cycle” in which tumor-induced bone destruction and bone microenvironment-driven tumor progression reinforce one another, underscoring an urgent need for novel strategies [8].