Re-examining the role of cytochrome c in cell death

When cytochrome c is released from mitochondria, it interacts with Apaf-1 to activate death-promoting caspases. Now, a gain-of-function mutation affecting cytochrome c with enhanced caspase-stimulatory activity is shown to have no other consequences for human health than a subclinical thrombocytopenia, showing that, in most settings, enhanced cytochrome c activity per se is not sufficient to disturb normal tissue homeostasis.