The association between cigarette smoking and development of lung adenocarcinoma increased gradually, and exposure to cigarette smoke not only promotes cancer cell progression and stemness but also reduces the sensitivity of NSCLC cells to EGFR TKI through several potential mechanisms, including EGFR hyperactivation, c-MET overexpression, and ABCG2-depednent drug efflux [9–12]. The gene discussed is EGFR; the disease is lung adenocarcinoma.