Since sCD13/B1R influences most cell types involved in RA, and inhibition of this interaction shows potent efficacy in ex vivo models of RA and animal models of arthritis, these results point to central roles for sCD13 and B1R in joint inflammation, and suggest that targeting sCD13 or its receptor could be a useful approach to the treatment of inflammatory diseases such as RA. This evidence concerns the gene BDKRB1 and rheumatoid arthritis.