In another investigation, overexpression of dickkopf-3 (DKK3) significantly enhanced ACE2 levels and promoted the degradation of AngII by inhibiting the phosphorylation of ADAM17, thereby reducing cardiac hypertrophy and fibrosis induced by AngII infusion in a mouse model with adenovirus-mediated DKK3 overexpression [104]. This evidence concerns the gene AGT and cardiac hypertrophy.