Recent studies have been suggested a cross-talk between angiotensin II (Ang II) and TLR4 in hypertension.43 It was reported that Ang II upregulated the TLR4 on mesangial cells and finally contributed to renal inflammation and fibrosis.44,45 Zhang et al46 demonstrated that TLR4 antagonist, TAK-242, reversed aldosterone-induced cardiac and renal injury. The gene discussed is AGT; the disease is hypertensive disorder.