It should be stressed that although a correlation was found to inflammation in RA, this was rather weak and, taken together with the different kinetics of response for CRP and COMP-C3b complexes after TNF-α inhibition, may suggest that the release of complexes is not merely due to inflammation but reflects other, yet unknown components of the disease process in RA (for example, being upstream of major cytokine release). This evidence concerns the gene CRP and rheumatoid arthritis.