Anemia is commonly complicated in patients with chronic kidney disease (CKD) and its incidence increases with the progression of the CKD stage. Anemia may cause a variety of complications in patients with CKD, including increased cardiac output, left ventricular hypertrophy, and a diminished immune response. Untreated anemia can further impair overall quality of life and increase the risk of requiring blood transfusions, cardiovascular (CV) events, hospitalizations, and death. Anemia occurs by multifactorial process in CKD. It is caused by a relative deficiency of erythropoietin (EPO), uremic-induced inhibitors of erythropoiesis, shortened erythrocyte survival, and dysregulation of iron homeostasis. Additionally, an excess of hepcidin has been implicated in the disordered iron homeostasis and anemia of CKD by impairing dietary iron absorption and iron mobilization from body stores. Most recently, a new class of medication, hypoxia-inducible factor-prolyl hydroxylase enzyme inhibitors (HIF-PHIs), has been suggested as an alternative therapeutic option for anemia in CKD. These agents  stabilize the HIF complex and stimulate endogenous EPO production even in patients with end-stage kidney disease. Moreover, HIF-PHIs have several advantages, including improvement of  iron mobilization to the bone marrow and oral administration which may be a more preferable route for patients not undergoing hemodialysis. As HIF-PHIs induce considerably lower but more consistent blood EPO levels than ESAs, they may be associated with fewer adverse cardiovascular complications with comparable hemoglobin levels, although this has yet to be evaluated in long-term clinical trials.   Given the high prevalence and poor prognosis of anemia in patients in CKD, additional treatment options with promising outcomes should be developed and implemented. In this session, recent practice and research in Korea on therapeutic aspects of anemia beyond EPO supplementation in patients with CKD patients will be discussed.