In addition, cytokines IL-6 and CCL2 released by SMCs may both promote the inflammatory milieu that characterizes aneurysmal disease.1 Indeed, following 6 hours of pulsatile pressurization expression levels of Mmp2, Mmp9, Il6, and Ccl2 were all significantly upregulated in stented aortas compared with unstented controls (Figure 3C), and this effect was spatially confined to the stiffness transition zone (interface zone) at the proximal end of the endograft (stent crown) (Figure 3D). The gene discussed is CCL2; the disease is Vascular dilatation.