During the pathogenesis of HUS, before the toxins act on the target endothelial cells of the kidney, several Stx forms are transported in the bloodstream: (i) soluble Stx [5,6]; (ii) Stx bound to circulating cells (neutrophils, monocytes, erythrocytes and platelets) exposing the receptors globotriaosylceramide (Gb3Cer) [7,8,9,10] and Toll-like receptor 4 (TLR4) [1,5], eventually inducing the formation of leukocyte–platelet aggregates and pathogenic extracellular vesicles; and (iii) Stx associated with blood-cell-derived microvesicles [5,10]. This evidence concerns the gene TLR4 and hemolytic-uremic syndrome.