accepted: 08/08/09; published on line: 08/10/09 E-mail: tony. donato@ colorado. edu Copyright:© 2009 Donato et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

NFκB is an important transcription factor expressed in all mammalian cell types. It is responsible for regulating gene expression of factors that control cell adhesion, proliferation, inflammation, redox status, and tissue specific enzymes. In arteries, NFκB is thought to promote CVD through its pro-inflammatory, proadhesion and pro-oxidant gene transcription. Recent evidence, however, suggests that not all NFκB-mediated gene regulation may be deleterious to the vascular system. For example, acute shear stress evoked increases in endothelial nitric oxide synthase, the enzyme that synthesizes the vascular protective molecule nitric oxide, is NFκB dependent [8]. The complexity in the control of NFκB signaling provides insight into how this transcription factor can have such diversity of regulatory responsibilities.