We further validated in our animal model of experimental status epilepticus that a decline in mitochondrial Complex I enzyme activity raised oxidative and nitrosative stress, and increased cytochrome c release from the mitochondria to the cytosol—thus triggering the activation of mitochondrial caspase cascades and leading to apoptotic cell death in the hippocampus [10,11,16]. This evidence concerns the gene CYCS and status epilepticus.