A recent study indicated that factor H inhibits the alternative pathway of complement activation, and a critical regulator of C3 activation in vivo, as well as factor H-deficient mice (Cfh-/-) mice spontaneously develop membranoproliferative glomerulonephritis (MPGN) that depends on C3 activation [40]. Here, C3 is linked to primary membranoproliferative glomerulonephritis.