(125) showed that GCK could inhibit osteoclast formation, which might be related to the molecular mechanism through inhibiting the JNK and ERK pathways, reducing the expressions of MMP-1, MMP-3 and RANKL in RA-FLS, and inhibiting RANKL-induced IκBα degradation and NFATc1, thereby inhibiting TRAP+ osteoclast-like cell formation. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.