In this work we provide mechanistic insight linking together two of the earliest observations in Parkinson's disease: the excessive build-up of iron in diseased substantia nigra neurons and mitochondrial dysfunction particularly increased reactive oxygen species production at the level of Complex I. We identify aconitase mutants as strong genetic suppressors of Parkinson-related pink1 mutant phenotypes, both at the organismal and at the cellular/mitochondrial level. The gene discussed is PINK1; the disease is Parkinson disease.