These include (i) a link between SARS and liver function abnormalities [74], (ii) the association of pulmonary iron overload and restrictive lung disease [49, 90, 91], (iii) the role of iron in pulmonary fibrosis [3], (iv) hepcidin’s modulation of the proliferation of pulmonary artery smooth muscle cells [107], and (v) the vital role of hepcidin in alveolar macrophage function [98]. This evidence concerns the gene HAMP and pulmonary fibrosis.