Researchers from the University of Osaka have demonstrated that mitochondrial hyperfusion, when induced by low levels of DRP1 or cellular stress, activates an immune response through the RIG-I–MAVS pathway. Dependent on the involvement of the BAX protein, the release of mitochondrial RNA into the cytosol enhanced natural killer cell cytotoxicity and reduced tumor growth in a xenograft model. The findings, published in Cell Reports, provide new possibilities for cancer research and treatment.