Consistently, reduced CFH bioavailability or activity, due to gene mutations or autoantibodies, may result in uncontrolled complement activation and consequent severe vascular damage, as observed in patients with atypical hemolytic uremic syndrome (aHUS), a rare thrombotic microangiopathy that targets the microvasculature of the kidney and other organs (Noris and Remuzzi, 2009). The gene discussed is CFH; the disease is atypical hemolytic-uremic syndrome.