It is conceivable that the high-level accumulation of HεdC on RA patients was due to imbalance of oxidative reaction over antioxidant defence system, impairment of DNA repair enzymes and/or excessive activity of 15-lipooxygenase or Cox-2, or the excess presence of 4-ONE or ω6 PUFAs in cell membranes. This evidence concerns the gene PTGS2 and rheumatoid arthritis.