SMAD2 and Myocardial fibrosis: 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.