Combining the observation that infiltrating neutrophils and Th17 form an inflammatory cross-talk with our previous findings that Cyr61 promotes Th17 development and FLS proliferation [28,29,46], we suggest that Cyr61 plays a key role in the vicious cycle formed by interaction among activated Th17, proliferated FLS and infiltrating neutrophils in the development of RA. Here, CCN1 is linked to rheumatoid arthritis.