This combination revealed a fully abolishment of the feedback survival stimulated by the AKT inhibitor through the decrease of EGFR, HER-2, and p-AKT, as well as a profound inhibition of 4E-BP1, resulting in amplified anti-proliferative and apoptotic effect in NSCLC cells. The gene discussed is EIF4EBP1; the disease is non-small cell lung carcinoma.