Interestingly, the MitoPark mouse, generated by direct deletion of mitochondrial transcription factor A (TFAM), which is needed for mtDNA replication, in DA neurons, is characterized by a marked deletion of mtDNA, impairment of oxidative phosphorylation, DA neuron degeneration, and motor deficits that mimic human parkinsonism [65]. This evidence concerns the gene TFAM and Parkinson disease.