A physiologically relevant animal model would need not only to recapitulate the dyslipidemia of human familial hypercholesterolaemia, but also produce the regulatory proteins and key components of human lipid metabolism that do not otherwise exist in mice, such as cholesteryl ester transfer protein (CETP) and apolipoprotein (a) (APO(a)). The gene discussed is CETP; the disease is metabolic syndrome.