Whilst the impaired production of hepcidin is known to be a direct result of the homozygous C282Y mutation and its effect on protein misfolding with the resultant absence of the HFE protein in the signaling pathway regulating hepcidin production, less than 40% of C282Y homozygotes develop hemochromatosis-associated morbidity and less than 25% develop advanced hepatic fibrosis3. The gene discussed is HAMP; the disease is hemochromatosis.