In light of the critical role of RAS dysfunction in the development of hypertension and our previous finding of increased AngII and AT1R in thoracic aortas of offspring with prenatal exposure to LPS30, we decided to explore the specific mechanisms responsible for RAS dysfuncton and its relationship with NF-κB activation in vascular tissue prior to the developmental onset of hypertension. The gene discussed is AGTR1; the disease is Hypertension.