The deletion of Atg7 in BrafV600E/+-driven lung cancer mice resulted in oxidative stress, which induced the antioxidant defense protein and nuclear factor erythrocytes-2-like 2 (NRF2), which accelerated tumor cell proliferation but reduced tumor burden at later stages of tumorigenesis and impaired tumor cell viability, thus increasing the survival of mice [41]. This evidence concerns the gene ATG7 and neoplasm.