Several studies have shown that reduced levels of APP and CP in PD patients lead to a decreased ability of FPN1 to export iron resulting in iron accumulation and oxidative stress production in the SN.[51,52] Transferrin was also found to significantly ameliorate motor deficits in the MPTP-induced PD mouse model by down-regulating DMT1 and ACSL4 and up-regulating FSP1, acting as a neuroprotective effect.[53]. The gene discussed is ACSL4; the disease is Parkinson disease.