Iron, an essential element for many important cellular functions in all living organisms, can catalyze the formation of potentially toxic free radicals. Excessive iron is sequestered by ferritin in a nontoxic and readily available form in a cell. Ferritin is composed of 24 subunits of different proportions of two functionally distinct subunits: ferritin H and L. The former is involved in ferroxidase activity necessary for iron uptake and oxidation of ferrous iron, while the latter is involved in nucleation of the iron core. The expression of ferritin is under delicate control and is regulated at both the transcriptional and posttranscriptional levels by iron, cytokines and oxidative stress. Elevated ferritin levels are associated with an increased risk of atherosclerotic coronary artery disease (CAD), the leading cause of death and illness in developed countries. Serum ferritin levels are a good indicator of iron stores in the body. In fact, epidemiological studies have suggested that elevated serum ferritin levels are associated with an increased risk of CAD and myocardial infarction (MI), though inconsistent results were obtained in some other studies. Moreover, recent proteomics and molecular biology studies have shown that ferritin levels in arteries are increased in diseased tissues, which further supports the link of ferritin to CAD/MI. Future studies will determine whether increased ferritin levels can serve as a distinct biomarker for the incidence of CAD/MI and distinguish whether increased ferritin levels are a cause of CAD or a consequence of the disease process.