Similarly, combination of oncogenic KRAS and TP53 loss triggered lung tumorigenesis and reliance on catabolism of branched-chain amino acids (BCAAs) as nutrients (Mayers et al., 2016) and KRAS has been shown to suppress p53 by activating the NRF2-regulated antioxidant defense system in human lung cancer cells (Yang et al., 2020). This evidence concerns the gene KRAS and lung cancer.