Consistent with the concept that mitochondrial fragmentation contributes to mitochondrial pathology, it is worth noting that a decrease in the protein levels of Drp1 has been reported in the SN, caudate and putamen of postmortem brain tissue from PD humans, data that is highly congruent with mouse models of PD [65], which underscores the need to use more than one complementary model of PD to study signaling pathways that regulate mitochondrial dynamics in the context of PD. The gene discussed is DNM1L; the disease is Parkinson disease.