STX1A and atypical hemolytic-uremic syndrome: Later, the model was supported by clinical investigations demonstrating the presence of Stxs detectable on neutrophils in the circulating bloodstream of pediatric D+HUS patients [204] and experiments showing that Stx1a binds at 100-fold lower affinity to neutrophil receptors in comparison to cells expressing Gb3, and using flow cytometry to show that FITC-conjugated Stx1a is transferred from neutrophils to glomerular microvascular endothelial cells stimulated with TNF-α [205].