As a proof-of-principle, the abrogation of HIPK2 activity by several means (silencing with small interfering (si)-RNA, overexpression of kinase-defective (KD)-mutant, HIPK2-knock-out (KO)) attenuates kidney fibrosis in Tg26 mice, as well as in other murine models of kidney fibrosis, such as unilateral urethral obstruction (UUO) and folic-acid-induced renal fibrosis, improving renal function and reducing proteinuria [67]. Here, HIPK2 is linked to renal fibrosis.