Concurrent depression of erythropoiesis by inflammation at the prevailing erythropoietin levels prevents the increase in erythroferrone release from erythroblasts that then opposes hepcidin effects on macrophages to mobilize their stored iron and increase gastrointestinal absorption of dietary iron.29 Together with iron deficiency, measurements of inflammatory markers and ESA response should become a part of management of resistant anemia in patients with NDD-CKD. This evidence concerns the gene EPO and Iron deficiency anemia.