Acrolein induced and accelerated atherosclerosis by promoting LDL-C-induced macrophage foam formation, stimulating ROS production[32–34], triggering the release of inflammatory factors such as IL-1β, IL-6, and TNF-α in HUVECs[35], as well as directly exacerbating the formation of atherosclerotic lesions in the aortic valve and aortic arch[32,36]. This evidence concerns the gene IL1B and atherosclerosis.