Mechanisms disrupting the barrier can range from EC dysfunction observed in the metabolic syndrome and cardiovascular disease, to EC de-differentiation upon withdrawal of critical stimuli like VEGF, observed in preeclampsia, to EC activation by inflammatory stimuli in HUS, TTP and sepsis, all the way to destruction of the EC in some forms of glomerulonephritis and vasculitis. This evidence concerns the gene VEGFA and hemolytic-uremic syndrome.