Excess hepcidin is known to impair dietary iron absorption in many CKD patients, thus providing a possible mechanism for anemia induction in our CKD models, moreover NGAL which is commonly used to determine kidney injury, is a mediator of iron sequestration, some studies showed that NGAL participates in the iron-depletion of the innate immune system [22,23]. The gene discussed is LCN2; the disease is chronic kidney disease.