Bcl-xL inhibits cytochrome-c redistribution from inter membrane space of mitochondria to cytosol by blocking both membrane hyperpolarization and mitochondrial swelling in response to several sets of apoptotic stimuli.65 Moreover, recent studies report that Bcl-xL protein interacts with Apaf-1 to inhibit the caspase activation involved in apoptosis,66 increases metastatic potential of breast cancer. This evidence concerns the gene BCL2L1 and breast carcinoma.