Previously, we have reported that hepatocyte growth factor (HGF), the ligand of the MET receptor, induces resistance to gefitinib or new generation EGFR-TKIs in EGFR mutant lung adenocarcinomas through the MET/Gab1/PI3K/Akt pathway, without involvement of ErbB3 [13, 14], although ErbB3 was critical in MET amplification–induced gefitinib resistance [15]. This evidence concerns the gene AKT1 and lung adenocarcinoma.