To evaluate whether the complement system and the C3a/C3aR axis were activated in the kidneys of mice with experimental HUS, we studied the deposition of C3—which implies local complement activation and the consequent generation of C3a by the C3 cleavage [36]—and the expression of C3aR in the renal glomerular and tubular compartments of C57BL/6 mice coinjected with Stx2 and lipopolysaccharide (LPS). The gene discussed is C3; the disease is hemolytic-uremic syndrome.