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. This evidence concerns the gene TNFRSF11B and rheumatoid arthritis.