However, in an AngII-induced hypertension model, AngII promoted Kruppel-like factor 5 (KLF5) expression and KLF5-myocardin binding, disrupted the feedback loop between ANO1 and myocardin, and then antagonised ANO1 transcription in human aortic SMCs, subsequently inducing cellular proliferation and vascular remodelling (51). The gene discussed is AGT; the disease is hypertensive disorder.