For example, atherosclerosis-prone apolipoprotein E (ApoE)-deficient (ApoE−/−) mice were subjected to variable chronic stress, and the mice then exhibited activated hematopoiesis and the promotion of atherosclerotic lesion features that are associated with vulnerable plaques that trigger stroke and acute myocardial infarction in humans [11, 12]. The gene discussed is APOE; the disease is stroke disorder.