Supporting the involvement of mitochondrial fragmentation in MPP+-induced mitochondrial dysfunction, several groups, including our own, have demonstrated that blocking DLP1 function by DLP1 knockdown or mitochondrial division inhibitors (i.e., mdivi-1 or p110 peptide) is sufficient to attenuate MPP+- or MPTP-induced mitochondrial dysfunction and neurotoxicity in PD cell culture and mouse models [23,31,32]. This evidence concerns the gene DNM1L and Parkinson disease.