In fact, our lab and others have postulated that the lower blood pressure observed in females in RAS-dependent models of hypertension is due to the ability of the female (in comparison to the male) to achieve lower plasma and tissue levels of Ang II (e.g., by increased catabolism of Ang II [39,49]) and/or through maintaining lower numbers of functional AT1Rs in the membrane of key target tissues like the kidney [50], which would result in less AT1R-mediated vasoconstrictor action in the female compared to the male (see excellent review by Sullivan [51]). The gene discussed is AGT; the disease is hypertensive disorder.