Further research shows that, FAPα+THY1+ fibroblasts mediate synovial inflammation by secreting cytokines and chemokines, while FAPα+THY1− plays a role in bone destruction by expressing osteoclast activity inducers consisting of matrix metalloproteinases, suggesting that synovial fibroblasts at different anatomical positions play different roles in the pathogenesis of RA. Here, FAP is linked to rheumatoid arthritis.