Since a gene-dosage imbalance of the Aph1b gene was the molecular-genetic basis of the APO-SUS/-UNSUS rat model [9] and the model was characterized by a disturbed endothelium-dependent vascular reactivity [6], [7], we tested the hypothesis that a genetic variation in the APH1B gene may contribute to atherosclerosis susceptibility in humans. This evidence concerns the gene AOPEP and atherosclerosis.