The therapeutic effect of LBP on STZ-induced DCM rats was documented previously (120), in which LBP abolished the STZ-induced myocardial damage, improved left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP), reduced the ratio of heart weight/body weight (HW/BW), and suppressed the expression level of serum atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), demonstrating that LBP may be an attractive treatment for myocardial hypertrophy and protect ventricular function. The gene discussed is NPPB; the disease is familial dilated cardiomyopathy.