In recent cohort studies, isolated low C3 level was found in only a proportion of patients with DDD4, 21 and C3GN.21, 42 C3NeF, first described in a patient with “persistent hypocomplementemic glomerulonephritis,”67 is an autoantibody that binds to a neoepitope on C3bBb, the C3 convertase of the AP, stabilizing it against complement factor H (Cfh)-mediated decay and prolonging its C3-cleaving action.68 This evidence concerns the gene CFH and glomerulonephritis.