Mitochondrial reactive oxygen species (ROS) exhibit context-dependent oncogenic roles: mtDNA mutations or electron transport chain defects induce ROS overproduction, activating nuclear factor kappa-B (NF-κB) and MAPK pathways to drive lung cancer metastasis (61), while pharmacologic ROS modulation exerts antitumor effects. The gene discussed is NFKB1; the disease is lung carcinoma.