In cancer tissues and cell lines, including lung, breast, and ovarian cancer cells, Nrf2 is highly expressed and activated due to either the oxidative microenvironment or genetic mutations resulting in loss of Keap1 function or gain of Nrf2 function as compared with that in normal cells [8–10]; thus, Nrf2 readily eliminates ROS from microenvironmental oxidative stressors, providing survival benefits. The gene discussed is KEAP1; the disease is cancer.