Elimination of properdin has been shown to be promising in mouse models of renal ischemia-reperfusion injury [101, 102], arthritis [52, 53, 103], allergic airway inflammation [99], abdominal aortic aneurysm formation [104], and, very recently, atypical hemolytic uremic syndrome (aHUS) [105]. The gene discussed is CFP; the disease is atypical hemolytic-uremic syndrome.