Moreover, they also found that SCD-EDS is attributed to a homozygous loss-of-function mutation in ZIP13 gene, and genetic analysis showed that the pathogenic mutation was a glycine to aspartic acid substitution at position 64 (G64D) in the ZIP13 protein, which is encoded by SLC39A13 [32]. The gene discussed is SLC39A13; the disease is Ehlers-Danlos syndrome.