Previous animal studies have demonstrated that modulation of the renin–angiotensin system (RAS) is the key mechanism in the development of CHTN-PE (Genest et al., 2013), and because renin is species specific for angiotensinogen cleavage, the overexpression of RAS in the uterus and placenta and the release of placental human renin into the circulation trigger preeclampsia-like symptoms in some rodents (Falcao et al., 2009). The gene discussed is REN; the disease is preeclampsia.