Several groups reported on the genetic polymorphism of the proteins involved in iron homeostasis, but not related to iron deficiency or overload . Genetic analysis of iron deficiency in mice has been evaluated . This study revealed that polymorphisms in multiple genes cause individual variations in iron regulation, especially in response to dietary iron challenge. In humans, genome-wide association studies found linkage of various gene polymorphism (single nucleotide polymorphism; SNP) and iron status, notably polymorphism of the gene coding for Mt2 [56, 120123]. Other investigators showed an association between Mt2 polymorphism and the risk to develop type 2 diabetes . The authors observed that individuals homozygous for iron-lowering alleles of Mt2 had a reduced risk of iron overload and of type 2 diabetes. In a genome-wide association study looking at heme iron uptake polymorphisms, no significant association with type 2 diabetes and iron metabolic pathways

An et al. presented evidence that genetic polymorphism of the Mt2 gene is associated with the risk to develop iron deficiency

Iron is a key player in hemoglobin synthesis an erythrocyte production. At the same time, it is a potent poison to mammalian cells and an indispensable nutrient for many diseasecausing germs and microbes. Therefore, its metabolism in mammalians is very complex and stringently controlled by many different genes and proteins. Identification of the genes and their polymorphic alleles may shed light into the metabolic interplay of relevant proteins. Ironomics may prove useful to better characterize patients with either iron deficiency or iron loading diseases. Finally, ironomics may be the ultimate goal for qualification and selection of individuals for blood donation according to their iron stores and of their capacity to maintain adequate iron metabolism despite supraphysiological iron depletion by blood donation.

Disclosure Statement BF and JDT received fees from Vifor Pharma. SWA, BF and JDT received research grants from Robapharm. BF also received research grants from Vifor Pharma. GW, CG, AB, and BMF declared no conflict of interest regarding this paper.