All this data demonstrated that prenatal inflammation exposure leads to the proneness of NF-κB activation at resting state and continued elevation of NF-κB activity results in suppressed PGC-1α rebound when facing a stressor challenge, which might be a pivotal factor implicated in vascular damage and progressive development of hypertension via an excessive oxidative stress mechanism. Here, NFKB1 is linked to hypertensive disorder.