Iron overload develops in circumstances in which control of body iron by regulation of intestinal iron absorption is either altered or circumvented. Genetic iron overload includes hereditary hemochromatosis, Juvenile hemochromatosis, African siderosis and others. Acquired iron overload occurs in a variety of conditions, it can be associated with repeated blood transfusions, end stage liver disease, hemolytic anemia particularly thalassemias and sickle cell anemia, and myelodysplastic syndromes. Porphyria cutanea tarda is a metabolic disorder recognized as a cause of secondary iron overload. The famous clinical manifestations of iron accumulation include liver disease, skin pigmentation, diabetes mellitus, arthropathy, impotence, and cardiac disease. The methods used to establish the presence of iron overload include iron studies, liver biopsy, and assessment of the response to phlebotomy. Regarding the diagnosis of iron overload, it can be suggested by symptoms and signs of iron overload, elevated transferrin saturation and serum ferritin concentration confirmed by the presence of parenchymal iron overload in liver biopsy. While treatment of primary hemochromatosis is mainly based on venesection, treatment of secondary iron overload is usually individualized, iron chelation with deferoxamine being the main line of therapy, the oral iron chelator, deferiprone, carries some hope especially in developing countries.