Preclinical evidence suggests that Akt activation may confer acquired resistance to EGFR inhibitors in EGFR mutant NSCLC.59 Similarly mTOR activation has been associated with EGFR and KRAS mutations and may act as a mechanism of resistance to EGFR inhibitors.60 Given the encompassing downstream signaling effects of the PI3K/Akt/mTOR pathway on the development and progression of malignancy, and its potential influence in response and resistance to standard therapies, it represents an attractive target for anticancer therapy in NSCLC. This evidence concerns the gene EGFR and non-small cell lung carcinoma.