The IL-1B-induced upregulation of OPG has far-reaching implications in cancer biology, where it highlights its immune evasion functions by allowing tumor cells to evade immune surveillance by the blocking of TRAIL by OPG, and further portrays the microenvironment support that IL-1B provides by recruiting inflammatory cells, promoting, neoangiogenesis, and enhancing stromal support through its role as a pro-inflammatory cytokine [39]. Here, TNFRSF11B is linked to neoplasm.