In summary, our results show that ectopic expression of constitutively activated Akt1 in NCI H460 human NSCLC cells can cause partial resistance towards a class of chemotherapeutics and may increase the apoptotic threshold or delay time course of certain apoptotic pathways, but does not completely suppress the activity of specified caspases or the chemotherapy-induced apoptosis. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.