HCN1 has been found to be higher with age in the MitoPark mouse, a genetic model of PD with disrupted mitochondrial function, perhaps as a compensatory effect to sustain firing rates and neural function.39 Our study also identified the expression of SLC4A4 (Na+‐coupled acid‐base transporter), EDN1 (endothelin‐1),40 and PCP4 (Purkinje cell protein 4) as higher in the dorsal SNpc neurons, all genes that maintain Ca2+ homeostasis and thus may be protective. This evidence concerns the gene HCN1 and Parkinson disease.