TNFSF11 and bone inflammation disease: Upon IL-1β stimulation, extracellular signal-regulated kinase (ERK) signaling is activated in the receptor activator of nuclear factor kappa-B ligand (RANKL)-induced OCs [24], which stimulates OC formation by activating the proliferation of OC precursors [25] and maintains the survival of OCs for bone resorption [26], provoking an excess of bone destruction under pathological conditions, such as in inflammatory bone diseases [27–29].