Combination of BYL719, a PI3Kα specific inhibitor, is able to overcome the resistance to gefitinib induced by PI3K/AKT activation in EGFR mutated NSCLC cell lines both in vitro and in vivo, and may be a new treatment strategy for EGFR mutated NSCLC patients with PI3K pathway aberrations. This evidence concerns the gene EGFR and non-small cell lung carcinoma.