However, the impact of the mitochondrial apoptotic pathway likely depends on the context including the cytotoxic stimulus, since we previously reported that XIAP inhibition combined with the death receptor ligand TRAIL can bypass BCL-2-imposed resistance of pancreatic carcinoma cells by switching type II cells, which depend on the mitochondrial contribution as an amplification step to the death receptor pathway, into type I cells in which TRAIL-induced caspase activation and apoptosis proceeds irrespectively of high BCL-2 levels [27]. Here, BCL2 is linked to exocrine pancreatic carcinoma.