Recapitulating the impact of “mitochondrial aging” in vitro, using juvenile cells has been challenging; however, we and others have previously shown robust phenotypes of LRRK2, PINK1, and Parkin mutant PD patient fibroblasts when subjected to low doses of small molecules which induce specific mitochondrial stress [10, 11, 18, 20]. The gene discussed is LRRK2; the disease is Parkinson disease.