In the present study, we found that CRP promotes RA pathogenesis via inducing RA-associated chromatin dysregulation that involved in both proinflammatory and OC-differentiation processes in peripheral monocytes, suggesting that targeting FRA2 could help protect against the aberrant activation of downstream genetic networks that contribute to RA pathogenesis following CRP-mediated chromatin dysregulation. This evidence concerns the gene FOSL2 and rheumatoid arthritis.