In a KRas-driven model of lung cancer, Atg5 deletion increased hyperplastic tumor foci formation, but decreased progression to adenocarcinomas and signs of malignancy [24]; in a Kras, p53−/− mouse model of lung cancer, Atg7 deletion altered tumor fate from adenomas to more benign oncocytomas, characterized by the accumulation of defective mitochondria [25]. The gene discussed is KRAS; the disease is lung carcinoma.