Vpr induces PPAR β/δ transcriptional activity, and increases phosphorylated PDH subunit E1α, leading to decreased activity of the PDH [13], an enzyme complex that plays a critical role in sodium transport in the renal tubule and contributes to the pathogenesis of hypertension in spontaneously hypertensive rats [14]. The gene discussed is DHTKD1; the disease is hypertensive disorder.