Different from most murine hypertension models (eg, defects in the renin-angiotensin-aldosterone system [RAAS]; deletion of eNOS),60,71,72 KI of human GYP.Mur increased murine erythroid AE1 and blood pressure moderately without overkilling other BP-regulating physiological systems. This evidence concerns the gene SLC4A1 and hypertensive disorder.