However, numerous tubular cells and α-SMA(+) myofibroblasts exhibited p-Smad3(+) or/and p-JNK(+) staining in biopsy specimens of IgA nephropathy (Figures 3F–J), suggesting that co-activation of Smad3 and JNK1/2 signaling in the tubulointerstitium persisted during the development and progression of CKD. This evidence concerns the gene SMAD3 and IgA glomerulonephritis.