Pedram et al. showed that estrogen prevents against myofibroblast development and production of collagen and fibronectin proteins that cause cardiac remodeling [4], while E2 reduces the turnover of ECM and exerts protective effects against cardiomyocyte apoptosis, estrogen withdrawal leading to left ventricular hypertrophy, collagen deposition, and increased sensitivity to constrictive agents, such as angiotensin II [31]. The gene discussed is AGT; the disease is left ventricular hypertrophy.