Finally, our data that Stx2 was able to enhance glomerular and tubular cell sensitivity to the adverse effects of C3a through the overexpression of its specific receptor are in strong agreement with the notion that Stx2 directly regulated complement activation, amplifying the detrimental effect of C3a/C3aR signaling at the renal level in HUS. Here, C3AR1 is linked to hemolytic-uremic syndrome.