Previous studies have shown that aged Polg mutator mice accumulate SNpc mtDNA deletions to a similar extent as that found in the SNpc in both PD patients and aged neurologically normal controls (∼50% of mtDNA molecules harboring deletions) (Bender et al., 2006; Kraytsberg et al., 2006; Perier et al., 2013). The gene discussed is POLG; the disease is Parkinson disease.