Published literature revealed that mitochondria from heterozygous (SOD2+/−) mice were partially deficient in MnSOD, showing increased proton leakage, respiratory depression, and mitochondrial oxidative damage, while liver mitochondria from homozygous mutant mice were completely deficient in MnSOD, showing significant respiratory depression and significant sensitization of mitochondrial permeability transition pores [54]. The gene discussed is SOD2; the disease is major depressive disorder.