Cancer therapies often kill cancer cells through mitochondrial apoptosis. Mitochondrial outer membrane permeabilization (MOMP) underpins apoptosis, leading to rapid caspase activation. Nonetheless, apoptosis is considered an immunosilent form of cell death, limiting its therapeutic effectiveness. Moreover, we and others have found that sub-lethal engagement of apoptotic signalling can have oncogenic effects. I will discuss how we can enhance the effectiveness of apoptosis by making it immunogenic. Investigating advanced prostate cancer as a treatment paradigm, we find that killing engaging MOMP under caspase inhibition engages anti-tumour immunity. Underlying this immunogenicity is the ability of permeabilized mitochondria to trigger inflammatory pathways, notably NF-kB and cGAS-STING, as the cell dies. I will discuss how damaged mitochondria engage inflammation and its biological roles, aiming to use this knowledge to improve cancer treatment.