In this regard, we believe it would be interesting to evaluate glomerulonephritis of different etiologies, such as IgA and membranous nephropathies, to support the hypothesis that protein milieu can induce the increase in APEMPs and to demonstrate whether the phenotypic changes in PECs, described in our research, are independent or not of the immunologic pathogenesis of the underlying nephropathy. The gene discussed is CD79A; the disease is glomerulonephritis.