It has been reported that patients with abnormal activation of phosphatidylinositol 3-kinase (PI3K)/AKT pathway, which can be induced by PIK3CA mutation/amplification, ErbB2 amplification, MET amplification, PTEN absence, or AKT amplification, usually have poorer clinical outcomes after EGFR-TKI treatment, despite of the sensitive EGFR mutation [5–9].In fact, about 15-48% EGFR-mutated NSCLC patients resistant to EGFR-TKIs harbored at least one genetic variation in PI3K/AKT pathway [8, 9]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.