We have recently shown in hypertensive Dahl SS (DS) rat, a paradigm of human SS hypertension characterized by cardiovascular injury and insulin resistance, that the upregulation of local (vasculature) Ang II activates the redox-sensitive transcription factor nuclear factor kappa (NFκB), which contributes to endothelial dysfunction, vascular inflammation, and the impairment of insulin-mediated vasorelaxation [13,15,16]. The gene discussed is AGT; the disease is endothelial dysfunction.