VPS35 and Parkinson disease: Familial PD-associated VPS35 mutants can cause mitochondrial fragmentation through enhanced VPS35-DLP1 interaction to recycle DLP1 complexes, eventually leading to mitochondria dysfunction and neuronal loss [18], and D620N mutant-induced mitochondrial fragmentation and respiratory deficits could be rescued by blocking the VPS35-DLP1 interaction and inhibiting the recycling of mitochondrial DLP1 complexes [30].