The most probable reasons for these results are: (i) the animals evaluated did not present either anemia or iron overload, but instead extremes from a normal biological distribution; (ii) The skeletal muscle is not the primary target either iron deficiency or overload [59]; (iii) Many genes from the iron metabolism pathways, such as Transferrin receptor 1, Divalent metal transporter 1, Ferroportin, Ferritin L and H, are post-transcriptionally regulated [2,70]. The gene discussed is SLC11A2; the disease is nutritional disorder.