The specific knockdown of Smad2/3 in activated fibroblasts can reduce the extent of cardiac fibrosis after pressure overload but cannot reverse myocardial hypertrophy and heart failure, whereas the specific knockdown of TGFBR1/2 can alleviate both cardiac fibrosis and hypertrophy (30). This evidence concerns the gene TGFBR1 and cardiac hypertrophy.