Most cases of aHUS are caused by uncontrolled complement activation due to genetic abnormalities in the alternative pathway, including complement factor H (CFH), complement factor I (CFI), membrane cofactor protein (MCP), thrombomodulin (THBD), complement component C3 (C3), and complement factor B (CFB) [6]. The gene discussed is THBD; the disease is atypical hemolytic-uremic syndrome.