To achieve specific chemogenetic inhibition of the STN neurons in the MitoPark PD model and potentially in humans, where the STN neurons do not express Cre or other recombinases to drive selective expression, we tested if we could achieve STN-specific expression of Gi DREADD in MitoPark mice by co-injection of cre-dependent Gi-DREADD AAV and AAV9-Vglut2-cre vectors into the STN. This evidence concerns the gene SLC17A6 and Parkinson disease.