In LDL receptor knock-out (LDLr−/−) mouse, as well as, in ApoE heterozygous deficient mouse, maternal hypercholesterolemia -induced either by diet or by cross-breeding wild type male mouse with ApoE deficient females- promoted atherosclerosis in aortic arch of the respective offspring [48], [49]. The gene discussed is APOE; the disease is familial hypercholesterolemia.