We show that a number of human NSCLC cell lines that are competent for interferon-γ (IFNγ) signaling (i.e. expressing IFNγ receptor-1 and STAT1) but have low expression levels of IAP proteins survivin and livin, can be readily killed through apoptosis by IFNγ and Smac mimetic co-treatment without harming normal human lung epithelial cells. The gene discussed is IFNG; the disease is non-small cell lung carcinoma.