SLC30A10 and polycythemia: Variants in genes linked to perturbations in metabolism provided readily accessible treatments; one patient’s congenital erythrocytosis was found to be a consequence of hypermanganesaemia caused by a missense variant in the manganese transporter SLC30A10. This gene would not have been routinely screened when erythrocytosis is the primary referral condition, although erythrocytosis is a known feature of these transporter defects due to inhibition of the iron centre of the hypoxia-inducible factor prolyl hydroxylase enzymes by the retained transition metals.