SLC39A13 and Schnyder corneal dystrophy: 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).