A carotid ligation model in ApoE-/- mice showed that disturbed flow, which contains low and oscillatory shear stress, induced endothelial dysfunction and enhanced smooth muscle cell proliferation, whereas gene expression of eNOS and of antiinflammatory transcription factors such as Krüppel-like factor 2 (KLF2) was downregulated in those regions of the arterial wall [24]. The gene discussed is KLF2; the disease is endothelial dysfunction.