The PI3K/AKT/mTOR pathway is deregulated in 50-70% of NSCLC (23, 24) by a variety of mechanisms including activating mutations in Anaplastic lymphoma kinase (ALK), Epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), Phosphoinositide 3-kinase (PI3K), or protein kinase B (AKT) (24, 25), by PIK3CA amplification, or by the loss of negative regulation through the tumor suppressor gene PTEN (26). This evidence concerns the gene EGFR and non-small cell lung carcinoma.