The results of these studies suggest the possibility that the inhibition of aberrant RANKL signaling in pathologic conditions would alleviate the progression of disc degeneration by downregulating catabolic factors, including proinflammatory cytokines and matrix-degrading enzymes, thus suggesting the potential use of OPG or monoclonal anti-RANKL antibody as a therapeutic agent against human IVD degeneration. The gene discussed is TNFSF11; the disease is intervertebral disk degenerative disorder.