Since splenic TFR2 protein could, by shedding of a soluble TFR2 form [47], theoretically influence the synthesis of hepcidin through interaction with the BMP pathway [48], and since the expression of liver TFR2 protein is posttranscriptionally regulated by iron status [49, 50], it was of interest to examine whether splenic TFR2 induction by EPO could be also modulated by iron overload or iron deficiency. This evidence concerns the gene EPO and nutritional disorder.