APOE and congenital bilateral aplasia of vas deferens from CFTR mutation: Consistent with these observations, the accumulation of NF-κB p65 in nuclei, expression of vascular cell adhesion molecule-1 (VCAM-1), and Mac3-positive macrophage content within the aortic valve were reduced by 50.8%, 46.8%, and 25.1%, respectively, in Apoe−/− mice treated with liraglutide (Figure 3D–F), whereas the expression of NOTCH1, a critical protein in controlling aortic valve calcification and CAVD in both mice and humans [12,13], was increased by 127% in liraglutide-treated Apoe−/− mice compared to saline-treated Apoe−/− mice (Figure 3G).