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Bax, when released from Bcl-2, will induce a mitochondrial permeability transition (MPT) in response to this oxidative stress [238], which will trigger cytochrome c to be released from mitochondria, activating caspase-mediated apoptosis [235]

Nonetheless, certain aspects of ASD symptomatology such as inflammation and oxidative stress seem to be shared by many ASD mouse models [19]