Thus, a major function of casp3/7 is to prevent inflammation driven by the cytoplasmic release of mtRNA, and by combining apoptosis-inducing cytotoxic or targeted chemotherapies with caspase-3/7 inhibition, it is possible to achieve the long sought-after goal of pharmacologically-induced, tumor-intrinsic, and cGAS/STING-independent Type I IFN production to potentiate anti-tumor immunity. This evidence concerns the gene STING1 and neoplasm.