Moreover, granulocytes from patients with psoriasis were also characterized by changes in the mitochondrial pathway including a decrease of the anti-apoptotic protein Bcl-2 that could lead to a release of cytochrome c from mitochondria that binds APAF1 and subsequently induces caspase-9, which results in the activation of caspase-3 and, thus, executes cell death [73]. Here, CASP3 is linked to psoriasis.