Furthermore, TNF-α and IL-1β are well accepted to induce osteoclastogenesis in osteoporosis, and inflammatory bone loss associated with rheumatoid arthritis and periodontitis.[21–23] These cytokines are also involved in the modulation of the OPG/RANKL system in patients with chronic liver disease.[21] Especially, TNF-α was known to induce osteoclastogenesis both dependently and independently via RANKL expression in OBs.[24,25] In the present study, a GGT specific antibody, AGT3, significantly suppressed GGT-induced upregulation of TNF-α and IL-1β expression in osteoblastic cells. The gene discussed is TNF; the disease is rheumatoid arthritis.