The hepcidin–ferroportin axis is central to systemic iron homeostasis and a dysregulation of hepcidin results in two phenotypically contrasting groups of clinical conditions: one in which increased hepcidin levels cause or contribute to iron-restrictive anaemias, and the other characterised by hepcidin deficiency, which results in iron overload, as observed in nearly all forms of hereditary haemochromatosis (HH) and iron-loading anaemias such as β-thalassaemia and congenital dyserythropoietic anaemias [4]. Here, HAMP is linked to hyperinsulinemic hypoglycemia, familial, 4.