Also, compromised basal, unstimulated NO release together with an intact receptor-stimulated NO response has been observed before in aortic segments of Fbn1C1039G/+ (Marfan model) mice [59], apolipoprotein E–deficient mice [60], stroke-prone spontaneously hypertensive rats [61] and warfarin-fed DBA/2J mice [20]. This evidence concerns the gene APOE and stroke disorder.