This possibility is supported by a recent report documenting homozygous SLC30A10 W275G variants in patients with neurological symptoms but without polycythemia or hypermanganesemia (26)—in these patients, neurological deficits are noted in the absence of blood Mn excess, suggesting that SLC30A10 mutations can have adverse effects without prominently perturbing Mn levels. Here, SLC30A10 is linked to polycythemia.