Low shear stress elicits an inflammatory response in arterial walls.5,17–18 Endothelial dysfunction with activation of proinflammatory and proliferative pathways is an integral part of the inflammatory response and involves activation of nuclear factor kappa B (NF‐kB),2 monocyte chemoattractant protein 1,1,19 and vascular cell adhesion molecule 1,10,20 among other inflammatory mediators. The gene discussed is CCL2; the disease is endothelial dysfunction.