Several studies have demonstrated that endogenous Dcn inhibits TGF‐β1 activation and reduced fibrosis in mouse lung and diabetic nephropathy models, as well as Dcn‐deficient models aggravated liver and kidney fibrosis via increased TGF‐β activation (Baghy et al., 2011; Kolb et al., 2001; Merline et al., 2009; Williams et al., 2007). The gene discussed is TGFB1; the disease is diabetic kidney disease.