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This observation supports the hypothesis that reticuloendothelial ironoverload in patients with ferroportin disease is caused by loss-of-functionmutations in the SLC11A3 gene that mainly impair macrophage ironrecycling.

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However, quantification of serumferritin awaited the purification of ferritin and anti-ferritin antibodies and the development ofsensitive immunoassay techniques.
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