Abstract: Apo(a) is a glycoprotein that underlies a large genetic polymorphism. Apo(a) is synthesized predominantly in the liver. After its synthesis, it binds with high affinity to the apoB binding site of LDL on the hepatocellular surface. Lipoprotein(α)［Lp(α)］ is degraded via LDL-receptor metabolic pathway and non-LDL-receptor metabolic pathway. Lp(α) is an important agent in the development of atherosclerosis and has some physiological functions in hemostasis, wound healing and angiogenesis. Lp(α) is an independent risk marker for coronary heart disease. Lp(α) plasma concentration is highly determined by genetic factors. However, plasma concentrations of Lp(α) are also affected by different diseases (e.g., diseases of liver and kidney), hormonal factors (e.g., sex steroids, thyroid hormones) as well as pharmaceuticals (e.g., nicotinic acid derivatives). This article focuses mainly on racial and sex differences of Lp(α) levels and influences of medication.