Evidence that osteoclast-like multinucleated giant cells are attached to eroded bone in inflammatory synovial joints suggests that osteoclasts play a crucial role in bone destruction in RA, which ultimately leads to joint deformity.[25] RANK interaction with RANKL on osteoclast precursor cells promotes cellular differentiation into activated multinucleated osteoclasts and the survival of osteoclasts with the capacity for bone resorption.[26,27] Osteoclasts that require activation of the RANK-RANKL signal pathway are also considered a potent therapeutic target in RA. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.