Hemin therapy also reduced LV hypertrophy, cardiac fibrosis, and cardiomyocyte longitudinal muscle-fiber thickness, a pathophysiological feature of cardiomyocyte hypertrophy [35], with a corresponding suppression of markers of heart failure such as osteopontin and osteoprotegerin [14, 15], as well as the reduction of extracellular matrix protein like TGF-β, fibronectin, and collagen which are implicated in cardiac hypertrophy and fibrosis [49, 57]. The gene discussed is TGFB1; the disease is cardiac hypertrophy.