The most common mutations of the EGFR gene found in NSCLC are deletions in exon 19 and the L858R mutation in exon 21, resulting in activation of EGFR and its downstream signaling pathways, such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), which has been proved to play an important role in the development, differentiation, survival and drug resistance of NSCLC (Wee and Wang, 2017). Here, MTOR is linked to non-small cell lung carcinoma.