While the rapid LRRK2 kinase mediated mtDNA damage reversal is a mitophagy independent process, future experiments with chronic LRRK2 kinase inhibition will encompass evaluating other facets of mitophagy-related pathways shown to be disrupted in LRRK2 PD model systems, including but not limited to impairment of PINK1/Parkin-dependent mitophagy signaling, aggregation and spatial arrest of damaged mitochondria to allow mitophagy initiation, and maturation of autophagosomes during mitophagy69,70,73. The gene discussed is PINK1; the disease is Parkinson disease.