However, under circumstances that result in longer term RAS activation, such as treatment with estrogen‐based contraceptives or during pregnancy, AGT may become rate limiting.38 By 11 weeks’ gestation, an additional high‐molecular‐weight form of AGT is identifiable in the plasma of pregnant women.39 Moreover, the proportion of high‐molecular‐weight AGT to normal AGT is also increased in women who develop pregnancy‐associated hypertension,40 suggesting a means by which continued RAS activation might underpin GH. The gene discussed is AGT; the disease is hypertensive disorder.