It can upregulate the density of β adrenoceptor in myocardial infarction rats to a level similar to that in normal rats, reduce the increase of atrial natriuretic factor (ANF) and connective tissue growth factor (CTGF) expression induced by myocardial infarction, retain myocardial contraction reserve, and inhibit cardiac remodeling to a certain extent, but will not change the changes of sarcoplasmic reticulum Ca2+—ATPase 2 and TGFβ1 expression induced by myocardial infarction (Burstein et al., 2007). The gene discussed is TGFB1; the disease is myocardial infarction.