This model demonstrated transient proteinuria, mesangial cell and matrix proliferation, mesangial IgA and C3 deposition and partial C3 subendothelial deposition by fluorescence immunostaining, as well as mesangial deposition and a hump in electron microscopy analyses, all of which are characteristics of both IgAN and IgA-dominant infection related to glomerulonephritis [101]. This evidence concerns the gene C3 and infection.