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Mitochondrial dysfunction is thought to contribute to Parkinson's disease progression, and factors that can overcome mitochondrial defects could potentially be used to combat the disease and prevent neuronal death. In this issue, Inoue et al 1 report that reduction of p13, a mitochondrial protein that inhibits complex I assembly, rescues the cellular and behavioral defects of Parkinson's disease models. This work suggests that stabilizing the mitochondrial electron transport chain may be beneficial in the context of Parkinson's disease.