Lung cancer cells are particularly sensitive to oxidative stress, as evidenced by the increased lung cancer risk observed in clinical trials of dietary antioxidants [1,2], frequent somatic mutations in nuclear factor erythroid 2-related factor 2 (NFE2L2, NRF2) or kelch-like ECH-associated protein 1 (KEAP1) that enhance production of endogenous antioxidants [[3], [4], [5]], and supporting mechanistic studies in mice [6,7]. This evidence concerns the gene KEAP1 and lung cancer.