Some studies have reported molecular mechanisms related to drug tolerance in EGFR mutant NSCLC, such as IGF-1R signaling activation, lipid hydroperoxidase glutathione peroxidase 4 (GPX4) dependency, aldehyde dehydrogenase (ALDH) upregulation, and the activation of β-catenin signaling, AXL or Aurora kinase A16–18. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.