The effects of CDDO-Me on mitochondrial dynamics and neuronal death has been studied in in the hippocampus, in a model of status epilepticus (SE) [51]: CDDO-Me increased the phosphorylation of DRP1 at Ser616 via the activation of extracellular-signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK), which facilitated DRP1-mediated mitochondrial fission and selectively attenuated SE-induced CA1 neuronal death. Here, DNM1L is linked to status epilepticus.