This observation support our in vivo findings in the models of AngII and hypertension-induced renal damage, both characterized by TGF-β1 overexpression and fibrosis in the absence of Notch pathway activation, as well as by the data in the model of UUO showing the lack of effect on renal Jagged-1 levels, but downregulation of TGF-β1 and renal damage, in response to AT1 antagonism. The gene discussed is TGFB1; the disease is hypertensive disorder.