These results suggest that production of RANKL and M-CSF by proliferating RA-FLS are not particularly dependent on NF-κB, and the suppressive effect of DHMEQ on osteoclastogenesis resulted from the downregulation of proosteoclastogenic factors other than RANKL, RANK or OPG. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.