Elevated hepcidin, stimulated by increased inflammatory cytokines and reduced renal clearance in CKD patients, prevented the use of absorbed iron and/or stored iron for erythropoiesis via the degradation of iron exporter ferroportin and the inhibition of cellular iron efflux [14,32], which consequently resulted in either functional or absolute iron deficiency to meet the demand for erythropoiesis [32]. Here, SLC40A1 is linked to chronic kidney disease.