Turnover studies of hepatic apoB using traditional analytic models showed that hepatic apoB is overproduced in HyperapoB, a finding which stands in marked contrast to the impaired catabolism of apoB in FH. A new multi-compartmental model of LDL metabolism has been developed which appears to elucidate several of the basic mechanisms involved in the pathogenesis of HyperapoB. All the data to date indicate that the characteristic abnormalities of LDL in HyperapoB are all consequences of the overproduction of hepatic apoB. Obviously, the goal for future research must be to understand the basis for this overproduction. A preliminary study with adipose tissue suggested that the overproduction of hepatic apoB might be secondary to a defect in peripheral tissue triglyceride biosynthesis.