[24], [25], [26] Li etc found that overexpression of NOTCH3 existed in the lungs of humans and rodents with pulmonary hypertension, knock-out mice with homozygous deletion of Notch3 did not develop pulmonary hypertension in response to hypoxic stimulation and pulmonary hypertension could be successfully treated in mice by administration of N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a γ-secretase inhibitor [24]. Also, our previous work found that DAPT could inhibit pulmonary vascular remodeling induced by angiotensin II and PDGF ex vivo [25], [26]. The gene discussed is AGT; the disease is pulmonary hypertension.