Although the different pathway taken by Cu entering the vesicular system via Atox1 compared to CCS-mediated loading of Cu into SOD1 may account for potential differences in the interactions of Cu with α-syn and SOD1 in PD, it remains unclear how MT could potentially intercept Cu as there is evidence that Cu is transferred directly from CTR1 to membrane-associated CCS (or likely also Atox1) [31]. The gene discussed is CCS; the disease is Parkinson disease.