Whether the observed changes to Purkinje cells in our FRDA cohort are solely a response to depleted cellular frataxin levels and/or loss of the dentate nucleus; or alternatively, at least in part, a result of secondary damage caused by hypoxic-ischemic injury (due to either cardiomyopathy or pulmonary complications as reported in our FRDA cases) cannot be fully determined. Here, FXN is linked to cardiomyopathy.