The concept that this mitochondrial dysfunction in PD leads to abnormal post-transcriptional regulation of iron homeostasis via IRP1 has also been confirmed in previous studies that showed the ferritin mRNA translation repression to be caused by sustained IRP1 activity in PD rodent models as well as patient brains [162,163], and that respiratory dysfunction due to complex I inhibition triggers decreases ISC-biogenesis and induces IRP1 activity [164]. Here, ACO1 is linked to Parkinson disease.