Genetic deletion of HIPK2 attenuated renal fibrosis development in various mouse models of renal fibrosis, which was associated with attenuation of TGF-β/Smad3-, Wnt/β-catenin-, and Notch-targeted genes 228, 234, and conversely, its overexpression results in exacerbated kidney injuries in experimental models of CKD and tubulointerstitial fibrosis 234-237. The gene discussed is SMAD3; the disease is renal fibrosis.