The synthesis of surface transferrin receptor is proportional to the iron requirement of the cell, as a response to insufficient supply of transferrin iron.3 In addition, soluble transferrin receptor provides an assessment of erythropoiesis status, because the increase in soluble transferrin receptor concentration is proportional to erythroid marrow expansion.1 Our results confirm these concepts, as iron-deficiency anemia and heterozygous beta-thalassemia showed soluble transferrin receptor concentrations that were higher than in the control group. The gene discussed is TFRC; the disease is Beta-thalassemia.