Recent work has found that mitochondrial ATP synthesis comes at the expense of rapid NAD+ regeneration, as generation of the proton gradient required by mitochondrial ATP synthase slows ETC electron flux and thus NADH oxidation.28 It would be interesting to assess whether tumor cells regulate Drp1 and Opa1 to maximize ETC flux and NADH oxidation at the expense of ATP synthesis, potentially through fission-mediated increase in proton leakage to counteract the slowing of ETC electron flux. This evidence concerns the gene OPA1 and neoplasm.