In the present study, we report a novel finding that IFNγ cooperates with Smac mimetics to trigger a profound apoptosis in a number of human NSCLC cell lines that are competent for IFNγ signaling (i.e. expressing IFNγ receptor-1 and STAT1) but have low expression levels of IAP proteins survivin and livin without harming normal lung epithelial cells. The gene discussed is STAT1; the disease is non-small cell lung carcinoma.