In addition, increasing evidence has been provided that extracellular Stx2(a)-bearing vesicles released in the blood of patients by toxin-challenged circulating cells (monocytes, neutrophils, and erythrocytes) and platelets are key factors in targeting renal endothelial cells and thus in the pathogenesis of HUS [146,147]. Here, STX2 is linked to hemolytic-uremic syndrome.