Our studies using the skin carcinogenesis model revealed that during early tumor promotion, the tumor suppressor p53 translocated to mitochondria and physically interacted with a primary antioxidant defense enzyme, manganese superoxide dismutase (MnSOD), leading to suppression of its superoxide scavenging activity, as well as, increases in ROS levels [52]. The gene discussed is SOD2; the disease is neoplasm.