Previous studies show that TLR4-mediated inflammatory response promotes Angiotensin II-induced cardiac hypertrophy and dysfunction[25].Several studies also indicate that inhibition of TLR4 improve cardiac function and attenuate myocardial fibrosis[24,26].However the role of TLR4 in aldosterone-induced cardiac damage is not clear. The gene discussed is AGT; the disease is Myocardial fibrosis.