In the context of kidney disease, we demonstrated that increased HIPK2 activity induces tubular cell injury and apoptosis through activation of the p53 signaling pathway and promotes renal fibrosis through enhancing TGF-β/Smad3, Notch, and Wnt/β-catenin signaling pathways (2, 3). Here, TGFB1 is linked to renal fibrosis.