Our results indicate mTORC2-associated signaling-pathway was hyperactivated in EGFR TKI-resistant cells and targeting mTOR with specific mTOR inhibitors is likely a good strategy for patients with EGFR mutant NSCLC who develop EGFR TKI resistance; the potential specific roles of mTORC2 in EGFR TKI-resistant NSCLC cells were still unknown and should be further investigated; and that expression of total or phosphorylated p70S6K may be a predictor of the response to mTOR inhibitors. This evidence concerns the gene MTOR and non-small cell lung carcinoma.