Recently, by using a sporadic model of CRC, Schwartz and colleagues showed that mice that are deficient in hepcidin, specifically in the colon tumor epithelium, exhibited diminished tumor number, burden and size as a result of the ability of hepcidin to degrade FPN1 and sequester iron, thus, sustaining the production of nucleotides and CRC cell proliferation [27]. The gene discussed is HAMP; the disease is colonic neoplasm.