IL-6 promotes the differentiation and maturation of Th17, and the synergistic effect of secreted IL-17 and TNF-α reduces NO production in the vascular endothelium and enhances blood vessel contraction; the release of IFN-γ regulates the production of local angiotensinogen in the kidney; subsequently, the AngII pathway and the renin-angiotensin-aldosterone system (RAAS) are overactivated, and the production of aldosterone increases, which enhances the reabsorption of water and sodium and aggravates high blood pressure [106–110]. This evidence concerns the gene AGT and hypertensive disorder.