Receptors for IL‐1β and IL‐18 are detected on monocytes, VSMCs and ECs.[14] A high level of IL‐18 has been found associated with carotid intima‐media thickening,[14] and the administration of IL‐18 to atherosclerosis‐prone apolipoprotein E‐deficient (ApoE−/−) mice has been shown to induce atherosclerosis and enlarge lesions, whereas a deficiency of IL‐18 was observed to attenuate atherosclerosis.[52]. This evidence concerns the gene APOE and atherosclerosis.