The underlying pathophysiologic impairment that is common in all forms of HH is hepcidin deficiency accompanied by FPN1 over activity due to mutations in the genes encoding hepcidin itself (HAMP) FPN1, or other elements of hepcidin regulation by iron such as HFE, TfR2 or HJV [9,134]. The gene discussed is SLC40A1; the disease is hyperinsulinemic hypoglycemia, familial, 4.