However, this regional specific effect of TRPC3 was found to change in aging monkeys and transgenic mice overexpressing human α-synuclein, where TRPC3 was found to become enriched in the mitochondria of striatal neurons and contribute to the disruption of mitochondrial membrane potential and cell apoptosis commonly seen in Parkinson’s disease (Chen M. et al., 2017). This evidence concerns the gene TRPC3 and Parkinson disease.