It is known that the regular consumption of alcohol is responsible for the disruption of normal iron metabolism in humans, resulting in the excess deposition of iron in the liver in approximately one-third of alcoholic subjects. The mechanisms involved are largely unknown; however, it is likely that the two major proteins of iron metabolism, ferritin and transferrin are intimately involved in the process. Tissue damage in alcoholic liver disease and the inherited iron-overload disease, haemochromatosis, are caused by excess alcohol and iron, respectively. The mechanisms of this damage are believed to be similar in both disease conditions and involve free radical-mediated toxicity. A high proportion of haemochromatosis sufferers consume excessive amounts of alcohol and synergistic hepatotoxic events may occur leading to the earlier development of liver cirrhosis. This review describes briefly the role of ferritin and transferrin in normal iron metabolism and in iron overload disease and explores the possible involvement of these proteins in the pathophysiology of excess iron deposition in alcoholic subjects.