Higher oxidative stress in tumors is thought to be caused by altered mitochondrial function and increased activity of reactive oxygen species (ROS)-generating enzymes such as cyclooxygenases, lipoxygenases, and NADPH oxidases, most of which are modulated by tumor-intrinsic factors including increased growth factor and oncogenic signaling (e.g., Ras signaling) and loss of tumor suppressor function (e.g., p53). The gene discussed is TP53; the disease is neoplasm.