The poor efficacy of first‐generation EGFR‐TKIs for lung adenocarcinoma appears to be related to the increased expression of CSC markers.282 Overexpression of shisa3 inhibited CSC properties in lung adenocarcinoma cells and reversed resistance to gefitinib/osimertinib, which are EGFR-TKIs.283 The EGFR-TKI, brexpiprazole, combined with osimertinib, is a potential therapeutic strategy for glioblastoma by chemosensitizing glioma CSCs through the downregulation of survivin expression.284. This evidence concerns the gene EGFR and glioma.