The findings of deficient total copper (mainly Cu (I)) in the LV coupled with substantively diminished CTR1 at the cell membrane, and with increased internalisation and lowered overall levels of the transporter, are consistent with a mechanism known to occur in several mammalian cell types, namely copper-evoked endocytosis [65,66] and degradation [65]: these findings are consistent with the presence of elevated Cu (II) in the ECM of the coronary vasculature in the diabetic heart, which could well trigger this defect [8] and thus cause heart failure in diabetes [16]. Here, SLC31A1 is linked to diabetes mellitus.