Thus the poorly perfused and hypoxic placenta is thought to synthesize and release increased amounts of vasoactive factors such as soluble fms-like tyrosine kinase-1 (sFlt-1), cytokines, and possibly the angiotensin II (ANG II) type 1 receptor autoantibodies (AT1-AA) and these are thought to induce widespread activation/dysfunction of the maternal endothelium in the vessels of the kidney and other organs that ultimately results in hypertension (8–10). Here, FLT1 is linked to Hypertension.