Uremic toxins caused oxidative and inhibited Ca2+ pump in erythrocytes which led to cytoplasm Ca2+ overload, resulting in erythrocyte apoptosis.73 Inflammation inhibited erythropoiesis by inhibiting the synthesis of erythropoietin, upregulating soluble erythropoietin receptors, and inducing erythroid progenitor apoptosis.71 Inflammation also accelerated erythrocyte destruction by activating macrophages.71 In addition, inflammation exhibited inhibition effects on the expression of transferrin and disturbed the ferric metabolism in erythrocytes, which may also be the cause of anemia.73 The gene discussed is EPO; the disease is anemia.