Previous studies found that NRF2 was essential for the activation of HO-1, GST, and NQO1, which contributed to the suppression of inflammatory response and oxidative stress with the reduction of cytokines (TNF-α, IL-1β) and lipid peroxidation (ROS and MDA), and improvement of antioxidant activity (SOD, CAT) in prostatitis [30–32]. The gene discussed is SOD1; the disease is urogenital neoplasm.