Importantly, MG132 treatment of the SCD-EDS patient cells increased the total ZIP13G64D protein expression to the level of healthy donors (Fig 4D, red line versus dotted line), indicating that the pathogenic G64D mutation of ZIP13 in SCD-EDS patients causes degradation of the functional protein by the proteasome-dependent pathway. The gene discussed is SLC39A13; the disease is Schnyder corneal dystrophy.