In KRAS-driven non-small-cell lung cancer (NSCLC), Gwinn et al. reported that mutated KRAS altered amino acid uptake and asparagine biosynthesis through ATF4 regulation under nutrient depletion, and that ASNS could contribute to apoptotic suppression, protein biosynthesis, and mTORC1 activation [27]. This evidence concerns the gene KRAS and non-small cell lung carcinoma.