This has to be evaluated in further studies, and in particular correlation needs to be observed between a durable fall in serum ferritin in response to weight control and exercise, and a correction in insulin Oleuropein resistance and reversal of fatty liver. The finding of steatosis and nuclear glycogen inclusions further support this theory, as it is a common finding in obesity and prediabetes. We did not find signs of primary liver disease. The frequency of hyperferritinemia not related to iron load is remarkable, as is the extreme male preponderance. Insulin resistance and metabolic syndrome is more prevalent in males, but not to the extent seen in this group. Confounding factors may have influenced patient selection, but hormonal effects and increased iron loss in females may also have been of importance. Selection bias on part of the referring physician is not possible to exclude. Possible explanations of hyperferritinemia among our patients might be that by binding iron, ferritin protects against formation of free hydroxyl groups, it could also be due to endothelial/ subendothelial inflammation or simply leakage of ferritin from hepatic cells. The frequency of hyperferritinemia in Norwegian unselected patient populations with insulin resistance is unknown, as are gender difference. The metabolic syndrome carries a well known increased risk for cardiovascular disease. Whether hyperferritinemia Columbianadin entails an additional risk is unknown. The greatest limitation of the study is the relatively small patient population, and male preponderance. The strength though, is the unselected patient population from a primary care hospital, and the performance of liver histology from most of the patients. In conclusion, the present study suggests that s-ferritin elevation in our patients is a marker of the metabolic syndrome with hepatic steatosis and insulin resistance, and not of iron overload. The direct pathogenic mechanism, however, remains unknown. Cancer is a heterogeneous, multi-step, complex genetic disease resulting from accumulated mutations. Cancers generally were considered to arise by the accumulation of an estimated 5�C7 causative mutations.