Loss-of-function mutations in CFH, MCP, and CFI or gain-of-function mutations in complement components factor B and C3 lead to undesirable complement activation in patients with atypical hemolytic uremic syndrome (aHUS), a microangiopathy characterized by microvascular endothelial activation, cell injury, and thrombosis [12],[13],[14],[15]. This evidence concerns the gene CD46 and atypical hemolytic-uremic syndrome.