C3 inhibitors could likely interfere with multiple pathogenic drivers in IA-HUS by simultaneously blocking the generation of C3-derived proinflammatory effectors (i.e., C3a) and also by attenuating the generation of terminal (lytic) pathway effectors that contribute to microvascular endothelial injury and inflammation (i.e., C5a, C5b-9) (68). This evidence concerns the gene C3 and hemolytic-uremic syndrome.