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Background: Iron (Fe) metabolism is dependent on heme biosynthesis in bone marrow erythroblasts and is strictly controlled. Failure of this process induces to absolute or functional iron deficiency anemia (IDA), which is common in general medical practice. Aim: This study summarizes the Fe role in normal and disturbed erythopoietic process and focuses on current biochemical indicators and available therapeutic options for Fe imbalance. Methods: A systematic review in PubMed, MedLine and MDConsult database was conducted. The research limits included English abstracts and full texts, referring to erythropoiesis, anemia and Fe during the last decade. Results: Erythrocyte delivers oxygen to the tissues, so the primary consequence of anemia is tissue hypoxia. Oxygen-sensing cells in kidney respond to hypoxia by increasing erythropoietin (EPO), the basic regulatory hormone of erythropoiesis. Fe is an essential micronutrient for adequate erythropoietic function. Anemia of chronic disease (ACD) and IDA are characterized by disturbances in Fe homeostasis. In addition, inflammatory disorders and renal insufficiency are complicated by severe depression of EPO levels. Red cell indices (hemoglobin, mean cell hemoglobin) and biochemical markers (ferritin, transferrin saturation and receptors) reflect hemoglobin biosynthesis and iron pathways. The therapy of underlying disease is essential in IDA and ACD, whereas adjuvant procedures are red blood cells transfusion, erythropoietic agents and Fe supplementation. Conclusion: The approach of Fe-deficient patient is complex and based on wide range of clinical and laboratory findings. The precise evaluation of them is critical for diagnosis and management modalities.