IS-induced Notch signalling in macrophages was shown to be functionally involved in driving atherosclerosis as Notch inhibition lowered IS-induced vascular phenotype and IL-1β expression in mice, which was translatable to CKD mice without additional IS supplementation where Notch inhibition lowered aortic plaque size and brachiocephalic artery stenosis [61]. Here, IL1B is linked to chronic kidney disease.