Delivery of the isolated RING0 domain and an engineered Parkin mini-peptide, designed based on its overlap with predicted protein binding sites within the RING0 domain, resulted in the correction of mitochondrial dysfunction observed by several functional measures that include reduced mitochondrial respiration, complex I activity, mROS production and mitochondrial membrane potential in neuroblastoma SH-SY5Y cells and hiPSC-derived neurons with endogenous, disease-causing mutations in PRKN. The gene discussed is PRKN; the disease is neuroblastoma.