The marked reduction of arthritic symptoms in CAIA mice, the changes in synovial tissue and joint bones from mice with CAIA after exogenous IFN-β intervention, and the effects of IFN-β on RA patients all support exogenous IFN-β administration as having immunomodulating effects on the CAIA model, and suggest it may reduce joint inflammation and, perhaps more importantly, bone destruction by inhibiting the RANKL-c-Fos signaling pathway activity. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.