To this list can now be added type II (CDG) congenital disorder of glycosylation [17] and Leigh-like mitochondrial disease [20]; both clinical disorders are associated with SLC39A8 variants of deficient Mn influx, resulting in defective Mn-dependent posttranslational glycosylation of proteins such as transferrin and β-1,4-galactosyltransferase [17, 20, 47]. Here, SLC39A8 is linked to congenital disorder of glycosylation.