Our understanding about hepcidin’s mechanism of action predicts that hepcidin elevation would be expected to sequester recycled and stored iron and prevent iron absorption, resulting in reduced iron availability for erythropoiesis and replenishing iron stores within liver and splenic macrophages, thus aiding in recovery from systemic iron deficiency (Casu et al., 2018, Aschemeyer et al., 2018; Ginzburg et al., 2018; Ginzburg, 2019; Figure 7). This evidence concerns the gene HAMP and nutritional disorder.