Insulin resistance syndromes can promote both atherogenesis and advanced plaque progression, and the mechanisms likely involve both systemic factors, particularly dyslipidemia, hypertension, and a pro-inflammatory state, but also the effect of perturbed insulin signaling at the level of the intimal cells that participate in atherosclerosis, including endothelial cells, VSMCs, and macrophages [31]. The gene discussed is INS; the disease is metabolic syndrome.