Notably, that a mutation in FPN (substitution of a serine residue for the cysteine residue at position 326) causes resistance to hepcidin binding and results in iron overload in vital organs.47–50 To further address the role of the “hepcidin-FPN regulatory axis” in osteoporosis, we generated a plasmid expressing the FPN-C326S point mutation. This evidence concerns the gene HAMP and osteoporosis.