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However, compelling evidence suggests that, for the majority of ROS-related anticancer drugs, apoptosis depends on the activation of the intrinsic pathway that involves mitochondrial PTPs, the permeability of which is increased with the cytoplasmic release of pro-apoptotic factors such as cytochrome c that forms a complex with apoptotic protease activating factor 1 (Apaf-1) and pro-caspase 9 to build the apoptosome, activating, in turn, effector caspases 77,78,79,80 (Fig