This hypothesis was directly supported by studies in a KRAS-mutant mouse model of lung adenocarcinoma; in fact, lung-specific IKKα deletion promotes KRASG12D-mediated lung adenocarcinoma development, in association with elevated NOX2, down-regulated NRF2, accumulated ROS and attenuated cell senescence [240]. The gene discussed is CYBB; the disease is lung adenocarcinoma.