Zhang et al. found that lacking Pkd1 exhibit extensive metabolic abnormalities, which include increased expression of iron importers DMT1, which in turn result in high iron levels, low GSH and GPX4 activity, increased lipid peroxidation, and propensity to ferroptosis in autosomal dominant polycystic kidney disease mouse models [14] Zeng et al. showed that a high expression DMT1, at the same time, the low expression of ferroptosis key factor GPX4 was detected in studying the benefits of iron chelators in the treatment of Parkinson's disease [15]. The gene discussed is GPX4; the disease is Parkinson disease.