Although a direct association between SH3BP2 and RA has not yet been identified [68], genetic variations that affect the expression level of SH3BP2 may be involved in the severity of bone loss progression in RA, because loss- and gain-of-function of SH3BP2 oppositely regulate RANKL-induced osteoclastogenesis [20], [23]. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.