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Because these patients’ symptoms — skull asymmetry, infantile spasms, dwarfism, brain atrophy, sensory impairments, and glycosylation abnormalities — resembled type II congenital disorder of glycosylation (CDG), this study established a link between Mn deficiency and hereditary CDG, showing that mutations in SLC39A8 can decrease the supply of Mn to the Golgi enzyme β-1-galactosyltransferase, which is essential for glycoprotein biosynthesis