Consistent with high concentrations of autoreactive antibodies, histology analyses of kidneys in Prkcd−/− mice indicate glomerulonephritis with mesangial cell proliferation and deposition of IgG and complement component C3, similarly to the findings of nephritis and reduced levels of C3 and C4 in some of the PKCδ-deficient patients [19, 21]. This evidence concerns the gene PRKCD and nephritis.