The PI3K-Akt-mTOR cascade is often hyper-activated in NSCLC, possibly due to various genetic alterations including phosphatase and tensin homolog (PTEN) depletion, PI3KCA mutation and sustained activation of different receptor tyrosine kinase [6, 27, 28, 39, 40]. This evidence concerns the gene MTOR and non-small cell lung carcinoma.