Blockade of DLL4-Notch signaling using an anti-DLL4 mAb (HMD4-2 hamster anti-mouse Dll4 IgG), attenuated the development of atherosclerosis, diminished plaque calcification, improved insulin resistance, and decreased fat accumulation in LDL-receptor-deficient mice fed with a high-fat, high-cholesterol, diet (244). This evidence concerns the gene DLL4 and atherosclerosis.