Although the binding affinity of Hcy to AT1R is significantly lower (105 times) than that of AngII, the circulating Hcy concentration, especially in HHcy condition, is however much higher (~5 log magnitude) than that of AngII [36]; therefore, Hcy-induced AT1R activation might add up the effects of AngII-AT1R activation in HHcy, finally promoting AngII-induced cardiac hypertrophy. The gene discussed is AGT; the disease is cardiac hypertrophy.