In summary, RA-FLSs exhibits abnormal proliferation, migration and invasive ability, and secretes a large number of pro-inflammatory cytokines and chemokines, which form a bidirectional feedback loop by regulating RANKL expression, metabolic reprogramming and other mechanisms, driving the abnormal activation of OC, which collectively disrupts the balance of bone metabolism and ultimately leads to bone erosion and joint destruction in RA patients. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.