In addition, we showed that endothelial deletion of CUX1 in the atherosclerosis-prone ApoE<sup>-/-</sup> mice blocks high-fat diet-induced senescence throughout the entire plaques, and these ApoE<sup>-/-</sup> mice exhibit similar phenotypes as the atherosclerosis-prone models with CTSL and Notch1/RBPJ inactivation including attenuated atherosclerotic lesion, intact and well-organized elastin fibers, and reduced macrophage content of plaque. Here, APOE is linked to atherosclerosis.