To verify whether FRA2 functions in the CRP-induced RA-associated chromatin dysregulation, we depicted the “footprint” of FRA2 and detected a higher DNA accessibility and a firmer TF occupation flanking FRA2 motifs in CRP-stimulated monocytes compared to unstimulated controls (Fig. 5e), implying a stronger DNA-binding activity of FRA2 after CRP stimulation. This evidence concerns the gene CRP and rheumatoid arthritis.