There is growing evidence in the literature to suggest that Smad2 is not a mediator of cardiac fibrosis, whereas Smad3 regulates of the secretory phenotype of myofibroblasts and has a detrimental effect on myocardial fibrosis.46, 47 We showed that FKBP12.6 overexpression did minor things in inhibiting the increased level of TGFβ1 expression, and phosphorylation‐Smad3 induced by AngII. The gene discussed is AGT; the disease is Myocardial fibrosis.