With this status epilepticus model, we demonstrated that activation of PPARγ increased mitochondrial UCP2 and superoxide dismutase 2, decreased mitochondrial translocation of Bax, reduced cytosolic release of cytochrome c through stabilizing the mitochondrial transmembrane potential, and lessened apoptotic neuronal cell death in the hippocampus [27]. This evidence concerns the gene BAX and status epilepticus.