Activation of the complement system was further confirmed by demonstrating the strong capacity of the patient's serum to induce C5b-9 deposits on cultured human microvascular endothelial cells ex vivo (Fig. 1G).[3] An extensive genetic screening found no mutation in the genes encoding the components of the alternative pathway of complement or its regulatory proteins known to be involved in atypical hemolytic uremic syndrome (aHUS), including CFH, CFI, MCP, C3, CFB, CFH-related proteins and THBD, and anti-CFH antibodies were not detected. The gene discussed is C3; the disease is atypical hemolytic-uremic syndrome.