In addition, experimental data indicated that Sema7A-Integrin-beta1 signaling itself promotes ERK activation, which can bypass the impact of EGFR-TKIs, featuring a candidate therapeutic target as well as a putative novel biomarker for predicting drug-resistance in patients with EGFR-mutated lung adenocarcinoma 86. This evidence concerns the gene EGFR and lung adenocarcinoma.