We postulated that: 1) the severity of colitis would not be exacerbated in the KOs, since (paradoxically) the intestinal epithelium is iron depleted due to high FPN1 iron export activity [32, 34–36]; 2) iron demand would be similarly increased in Hamp-/- rats during acute intestinal inflammation (to support the immune response and tissue regeneration); and 3) increased demand for iron could be met (at least in part), by release of storage iron (which is at maximal capacity in these rats). This evidence concerns the gene HAMP and colitis.