This model then induced cardiac pressure overload via aortic constriction (an in vivo methodology to induce cardiac hypertrophy and heart failure) and it was found that deletion of Smad3, Smad2/3 or Tgfbr1/2 was able to inhibit cardiac fibrosis following aortic constriction [80]. The gene discussed is TGFBR1; the disease is cardiac hypertrophy.