50). Targeting the TGF-β/Smad3 signalling pathway is a potential therapeutic approach for myocardial fibrosis. Research using a mouse model involving the selective deletion of Tgfbr1/2, Smad2, or Smad3 in fibroblasts revealed that while deleting Tgfbr1/2 reduced fibrosis, deleting Smad2 did not significantly alter the fibrotic response. However, deleting Smad3 markedly decreased fibrosis, suggesting that Smad3 is more efficient than Smad2 in activating fibroblasts during cardiac fibrosis (Ref. 50). This evidence concerns the gene TGFBR1 and Myocardial fibrosis.