Proinflammatory cytokines including TNF-α, IL-17, IL-1β, and IL-6, derived from synovial fibroblasts of inflamed joints, are the primary trigger for the local or systemic high expression of RANKL in mice and RA patients [7, 8], which is one of the main mechanisms of inflammation-induced bone loss in RA. The gene discussed is IL17A; the disease is rheumatoid arthritis.