In our recent works, we showed that sustained seizures prompted the overproduction of nitric oxide, superoxide anion, and peroxynitrite formation that compromised mitochondrial respiratory chain enzyme activity, particularly in Complex I, and mitochondrial ultrastructure damage that caused cytochrome c/caspase-3-dependent apoptotic cell death in the hippocampal CA3 subfield following experimental status epilepticus [10,11,16]. The gene discussed is CASP3; the disease is status epilepticus.