Pharmacological or genetic inhibition of fumarate hydratase, which converts fumarate to malate, increased the intracellular levels of fumarate and, in turn, activated the RLR‐MAVS and cGAS‐STING pathway.[47, 50] Moreover, the mitochondrial membrane integrity was reduced or lost during sub‐lethal genotoxic stress, linking DNA damage‐induced type I IFN to the release of gDNA and mtDNA/mtRNA.[46] Thus, mitochondrial health may co‐regulate the efficacy of PARP7i in inducing apoptosis and anti‐tumor immunity. This evidence concerns the gene DHX58 and neoplasm.