In addition to transfusion burden in the past, IO in non‐transfusion‐dependent patients with hereditary anaemias, such as beta‐thalassemia and congenital dyserythropoietic anaemia, is often the result of ineffective erythropoiesis, where high levels of erythroferrone inhibit hepcidin production [5]. The gene discussed is HAMP; the disease is Beta-thalassemia.