Since CB1R inverse agonism by rimonabant improves atherogenic dyslipidemia in mice (12, 13, 14) and humans (20), in the current study, we aimed to investigate whether rimonabant attenuates atherosclerosis development using hyperlipidemic E3L.CETP mice, a well-established mouse model for human-like lipoprotein metabolism because of an intact ApoE-LDLr pathway. The gene discussed is APOE; the disease is metabolic syndrome.