Recent studies, furthermore, link tubular epithelial dysfunction in response to both acute (e.g., ischemia-reperfusion, nephrotoxins) and more protracted (UUO) injury to the progression of renal fibrosis via the p53 and JNK pathways with the retention of TGF-β signaling (Yang et al., 2010). Here, TP53 is linked to renal fibrosis.