Thus, mouse models of atherosclerosis, like those with genetic deletion of ApoE or the LDL receptor, have been successfully used to elucidate mechanisms of action in human atherosclerosis, but many mouse models of metabolic syndrome and diabetes, such as the Zucker diabetic fatty rat, do not show similar profiles of dyslipidemia to humans and do not develop atherosclerosis [148]. The gene discussed is LDLR; the disease is metabolic syndrome.