Moreover, some studies have revealed an interaction between members of the Nrf2 and NF-κB pathways, since that oxidative stress-induced NF-κB activation plays a pivotal role in the pro-inflammatory overproduction factors associated with the pathogenesis of RA and the activation of the Nrf2/ARE system disrupts this cycle [44]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.