Similar studies have not been performed with ACPA or RF, but the arthritogenic anti-CII mAb react with surface-exposed epitopes on CII that contain arginine, and equivalent ACPA mAb reactive with the citrullinated epitopes have been derived that enhance the development of arthritis [50,72], and may well have similar disruptive structural effects. This evidence concerns the gene PRTN3 and arthritic joint disease.