Familial combined hyperlipidemia (FCHL) is the commonest form of hereditary hyperlipidemia (1, 2). Its primary defect is increased secretion of hepatic triglyceride (TG)-rich apolipoprotein B (apo B)-containing particles (VLDL)(3) and impaired clearance of postprandial lipoproteins (4), which increases the number of circulating TG-rich lipoproteins. FCHL is present in up to 20% of survivors of myocardial infarction, and it is considered a significant genetic risk factor for developing cardiovascular disease (1, 5). The underlying genetic defect is unknown, although the disease has been linked to chromosomes 1 (6) and 11 (7). With regard to the latter, linkage