We report an atypical disease course initially resembling HUS, which was later interpreted as a severe complement-mediated hemolysis with C3 hypocomplementemia, triggered by a severe bacterial infection (Bordetella parapertussis) and exacerbated by C3NeF (the two-hit immunopathology hypothesis)—a novel sort of bystander hemolysis (5, 7). This evidence concerns the gene C3 and hemolytic-uremic syndrome.