Future investigations of the molecular details underlying the degradation of G64D and ΔFLA mutants, and of the protein structure and homeostasis of ZIP13, will provide a framework to develop potential treatments for SCD-EDS and for the related metabolic diseases since ZIP13 is also implicated in adipose and muscle tissues homeostasis (Fukada et al, 2008). This evidence concerns the gene SLC39A13 and Other metabolic disease.