The importance of the RANKL/RANK/OPG system in the development of bone destruction in RA has been recently established, since RANKL is highly expressed in the synovial tissue of RA patients (33–35) and inhibition of RANKL with denosumab results in amelioration of bone destruction in RA (36, 37). Here, TNFRSF11B is linked to rheumatoid arthritis.