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High levels of mitochondrial DNA deletions have been found in dopaminergic neurons of§Parkinson Disease patients, suggesting a role in the pathology. However, the reason for this§accumulation of mtDNA deletions is unclear. In this work, dopamine was found to drive this§phenomenon, probably through forcing continuous DNA strand-break repair events. The§results also suggest that mtDNA deletions are acting in combination with other cell-specific§factors, to promote neurodegeneration.