Interestingly, even though both cardiac fibroblast-specific deletion of Tgfbr1/2 and Smad2/3 significantly reduced cardiac fibrosis induced by transverse aortic constriction (TAC), only the deletion of Tgfbr1/2 in cardiac fibroblasts ameliorated cardiac hypertrophy and resulted in a functional improvement at 4 and 12 weeks after TAC (Khalil et al., 2017). The gene discussed is TGFBR1; the disease is cardiac hypertrophy.