In STZ-induced diabetic ApoE−/− mice, impaired capillarization and perfusion of the ischemic hindlimb has been reported [55]; however, when arteriogenesis was compared in mouse models of T1D (STZ-induction and the NOD mice), insulin resistance (ob/ob), and hypercholesterolemia (ApoE*3-Leiden mouse), hypercholesterolemia was found to be by far the more effective stimulus for reducing collateral arterial growth [56]. The gene discussed is APOE; the disease is familial hypercholesterolemia.