The pathophysiology of RA is associated with alterations in the cytokine network (mainly interleukin 6), a large increase in acute-phase reactants (including serum C-reactive protein, hepcidin, and ferritin), and certain autoantibodies (rheumatoid factor and anti-cyclic citrullinated peptide antibodies) [2,3]. Here, CRP is linked to rheumatoid arthritis.