Moreover, IL-34 activated/inhibited the expression of RANKL/OPG by fibroblast-like synoviocytes and circulating monocytes promoting cartilage and bone destruction in an IL-17-dependent manner, which was consistent with the correlation observed between increased IL-34 and RANKL levels in patients with RA 117,118. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.