They found that complement activation in AAV occurs predominantly via the alternative pathway.[29] In C3GN, C3Nefs can stabilize C3 inverters by prolonging their half-life, increasing C3 fragmentation, and thereby decreasing serum complement C3 levels; moreover, abnormal complement regulatory proteins can also lead to excessive activation of complement alternative pathways.[30] Aadel Chaudhuri et al reported a case of C3GN co-occurring with GPA, but this diagnosis remains unclear as the incidence of GPA is high and other reports have described cases of GPA with glomerular immune deposits. The gene discussed is C3; the disease is granulomatosis with polyangiitis.