A review of the topic of histone deacetylase inhibition in NSCLC indicated that a SIRT1-mediated survival advantage may represent another mechanism through which NSCLC cells develop resistance to EGFR-TKIs (109), possibly through mediated by regulating the oxidative phosphorylation of mitochondria in lung adenocarcinoma cells, and then selectively eliminating TKI-resistant cancer stem cells. This evidence concerns the gene EGFR and lung adenocarcinoma.