During the pathogenesis of cerebral ischemia/reperfusion injury, mitochondria play a critical role in promoting apoptosis via the reduction of mitochondrial membrane potential, the depletion of ATP synthesis, and the induction of increased membrane permeability.39, 40, 41 As a result, cytochrome C molecules are released from the mitochondria into the cytosol, to form a complex with Apaf-1, which binds to caspase-9 and activates it. Here, APAF1 is linked to brain ischemia.