Mitochondrial apoptosis is mediated by BAK and BAX, two proteins that oligomerise in the mitochondrial outer membrane to induce permeabilization, leading to cytochrome c efflux and activation of apoptotic caspases. Recent evidence indicates that, in the absence of active caspases, mitochondrial (mt) DNA triggers the innate immune cGAS/STING pathway, causing dying cells to secrete type I interferon. How cGAS gains access to mtDNA remains unclear, particularly since BAK/BAX are not thought to permeabilize the organelle’s inner membrane. Using a combination of live-cell lattice light sheet (LLSM), 3D-structured illuminated (SIM), correlative light electron microscopy (CLEM) and electron cryotomography (ECT) we have examined mitochondrial morphology during apoptosis. We document the formation of BAK/BAX macropores and extrusion of the inner mitochondrial membrane through them, an event we term “mitochondrial herniation”.