Placental ischemia, in turn, promotes disproportionate emission of anti-angiogenic agents [as soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng)] and pro-angiogenic agents [as placental growth factor (PLGF) and vascular endothelial growth factor (VEGF)], stimulated inflammatory cells releasing autoantibodies and inflammatory cytokines and increased oxidative stress which contribute significantly to generalized maternal endothelial dysfunctions in various organ beds, leading to hypertension, renal endotheliosis and blood coagulation (Gathiram & Moodley, 2016). This evidence concerns the gene FLT1 and hypertensive disorder.