Collectively, our data demonstrate that both PI3K-Akt-mediated degradation of IκBα and impaired NF-κB self-negative feedback loop on newly IκBα re-synthesis implicates in IκBα down-regulation and NF-κB over-activation in conduit arteries, leading to hypertension in the offspring exposed to an inflammatory stimulus during the prenatal period. Here, AKT1 is linked to Hypertension.