They suggested that the finding was due to an increase in the level of Th17 in T cells and an increase in the IL-17 level following infusion of chronic angiotensin II, an increase in superoxide radicals due to deposition of IL-17 on vessel walls, a decrease in endothelium-related vasodilatation, and some affected genes (e.g. stanniocalcin-1), which caused HT and vascular inflammation. The gene discussed is STC1; the disease is hematocrit.