Studies of the RA animal model have shown that the expression of RANKL is upregulated in inflammatory joints [20–24]; the level of secreted osteoprotegerin (OPG), a TNF receptor-related protein, is decreased; and the ratio of RANKL to OPG is positively correlated with osteoclast activity and local bone erosion. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.