During the early stage of atherosclerotic lesion formation in Apolipoprotein E (Apoe)-deficient mice, the HAS3 expression is increased and controlled in vascular smooth muscle cells by the cytokine IL-1β [46], and even if data on endothelial cells are unavailable, there are clear indications that HAS3 might be a promising therapeutic target in atherosclerosis. Here, IL1B is linked to atherosclerosis.