The hyperlipidaemic profile of the ApoE model is mainly driven by cholesteryl-ester rich VLDL remnants and thus exhibits a vastly different metabolic pathophysiology compared to the typical lifestyle-induced dyslipidaemia seen in humans, which is mainly caused by elevated levels of ApoB-100 rich LDL-cholesterol [34]. The gene discussed is APOE; the disease is inherited lipid metabolism disorder.