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34 reviewsMany anticancer agents induce apoptosis, mitotic catastrophe or cellular senescence. Here, we report the functionalcharacterization of an experimental inducer of tumor necrosis factor (TNF)-independent necrosis, necrocide-1 (NC1). NC1 (but notits stereoisomer) killed a panel of human cancer cells (but not normal cells) at nanomolar concentrations and with a non-apoptotic,necrotic morphotype, both in vitro and in vivo. NC1-induced killing was not inhibited by caspase blockers, anti-apoptotic BCL2overexpression or TNFα neutralization, suggesting that NC1 elicits a bona fide necrotic pathway. However, pharmacological orgenetic inhibition of necroptosis, pyroptosis and ferroptosis failed to block NC1-mediated cell death. Instead, NC1 elicited reactiveoxygen species (ROS) production by mitochondria, and elimination of mitochondrial DNA, quenching of mitochondrial ROS, as well1234567890();,:as blockade of mitochondrial permeability transition with cyclosporine A, interfered with NC1-induced cell death. NC1 inducedhallmarks of immunogenic cell death incurring calreticulin (CALR) exposure, ATP secretion and high mobility group box 1 (HMGB1)release. Taken together, these data identify a previously uncharacterized signaling cascade leading to an immunogenic variant ofmitochondrion-regulated necrosis, supporting the notion that eliciting regulated necrosis may constitute a valid approach foranticancer therapy.Cell Death and Disease (2023) 14:238 ;