Said another way, although we do not yet understand the pathophysiological mechanism that enables persistent erythropoiesis in PV despite iron deficiency, we anticipate that using hepcidin mimetics to further suppress iron absorption and recycling may prevent erythropoiesis in PV, redistributing iron to non-hematopoietic cells and possibly reversing iron deficiency associated symptoms in PV patients. This evidence concerns the gene HAMP and acquired polycythemia vera.