Experimental studies of gene deletion and pharmacological activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that coordinates basal and inducible expression of enzymes protective against oxidative stress and dicarbonyl glycation [36, 37], supports a role of oxidative damage and dicarbonyl glycation in the development of OA and RA [38, 39]. The gene discussed is NFE2L2; the disease is rheumatoid arthritis.