Among these models were wildtype normolipidemic mice transplanted with atherosclerotic arterial segments from Apoe−/− mice [13]–[18], Apoe−/− mice treated with apoE-encoding adenoviral vectors [19], Ldlr−/− mice treated with an microsomal triglyceride transfer protein (MTP) inhibitor [20], and mice that have a plasma lipid profile similar of that of hypercholesterolemia (Ldlr−/−Apob100/100) and a genetic switch to block hepatic synthesis of lipoproteins and thereby lower plasma lipoproteins (Mttpflox/floxMx1-Cre) [21]–[23]. The gene discussed is MTTP; the disease is familial hypercholesterolemia.