Afatinib combined with EA in NSCLC was studied due to two main reasons: one is a paper which revealed that β-catenin of the classical WNT signaling pathway contributed to lung tumor development induced by EGFR-T790M mutations, and genetic deletion of β-catenin gene dramatically reduced lung tumor formation in EGFR-L858R-T790M transgenic mice [15], and the other one is EA as a glutathione S-transferase P1-1(GSTP1-1) and WNT inhibitor can improve the antitumor effects of irreversible EGFR TKIs in breast cancer [14]. The gene discussed is GSTP1; the disease is breast carcinoma.