KLF2 expression is induced by laminar shear stress and inhibited by proinflammatory cytokines in endothelial cells.24, 42 Sustained overexpression of KLF2 induces endothelial nitric oxide synthase and thrombomodulin expression, and reduces cytokine-mediated activation of proinflammatory genes.43 Hemizygous deficiency of KLF2 increases diet-induced atherosclerosis in apolipoprotein E-deficient mice. The gene discussed is APOE; the disease is atherosclerosis.