The development of secondary glomerular sclerosis in IgAN, as a consequence of IgA1 immune deposition, stimulation of mesangial cells, subsequent release of cytokines and inflammatory mediators responsible for the mesangial–podocyte cross talk, which induce podocyte injury, maybe totally different from the development of focal segmental glomerulosclerosis in other primary glomerulonephritis such as membranous or membranoproliferative glomerulonephritis [19–23]. Here, IGHA1 is linked to glomerulonephritis.