The metabolic requirement for glutaminolysis may also similarly manifest as a therapeutic vulnerability in other cancers with genetic (132–137), epigenetic (138–140), or post transcriptional (141) alterations in the KEPA1/NRF2 signaling pathway, a hypothesis that illustrates the importance of kinase-targeted therapeutic strategies for KRAS-KEAP1 mutant lung cancer (142). This evidence concerns the gene KEAP1 and lung cancer.