Although TGF-β activates both Smad2 and Smad3 in vivo, CF-specific Smad2/3 knockout mice demonstrated that the observed effects on cardiac fibrosis and scar formation following pressure overload or myocardial infarction, respectively, were mainly attributed to Smad3 [70,71,72]. This evidence concerns the gene SMAD2 and myocardial infarction.