This may be result from genetic mutations of proteins involved in the pathway such as CFH, complement factor I (CFI), and complement factor H related proteins (CFHRs).[9] However, it is thought that genetic defect alone may not be sufficient to initiate the disease in many patients.[2,4] A trigger factor that targets one of the components of the pathway is often required for the development of C3 GN, such as C3NeF, an autoimmune antibody against C3 convertase,[10] and antifactor H antibody, which targets CFH. The gene discussed is CFH; the disease is ganglioneuroma.