However, if this were the case, then Hfe-/- mice with lower expression of Sfxn2 than wild-type mice would have reduced levels of Alas co-factor in the mitochondrion and have lower efficacy of heme biosynthesis, thus leading to the inappropriate iron-deficiency signal and the consequent upregulation of intestinal iron absorption. This evidence concerns the gene SFXN2 and Iron deficiency anemia.