We found that IFNγ could cooperate with various Smac mimetics to trigger a profound apoptosis in a number of NSCLC cell lines that are competent for IFNγ signaling (i.e. expressing IFNγ receptor-1 and STAT1) but have low expression levels of inhibitor of apoptosis proteins survivin and livin without harming normal human lung epithelial cells. This evidence concerns the gene IFNG and non-small cell lung carcinoma.