The first inborn error of manganese metabolism has recently been identified.1 This autosomal recessive condition caused by mutations in the SLC30A10 (Solute Carrier Family 30, Member 10) gene, encoding a manganese transporter, results in manganese accumulation, mainly in the basal ganglia and cerebellum, and the liver, and causes a syndrome of early-onset generalized dystonia, cirrhosis, polycythemia, and hypermanganesemia.1–3. Here, SLC30A10 is linked to polycythemia.