In contrast, knockdown TGFβR2 in both myocardial fibroblasts and cardiomyocytes has been shown to effectively inhibit both classical and non-classical TGFβ pathways, providing significant protection against afterload-induced cardiac fibrosis, myocardial hypertrophy, and ventricular dysfunction 32-34. The gene discussed is TGFBR2; the disease is cardiac hypertrophy.