More importantly, cardiomyocyte-specific overexpression of human GCH1 gene favorably regulates BH4, the dimerization and phosphorylation of neuronal NOS (nNOS), free Ca2+ and SR Ca2+ release in cardiomyocytes, and the expression of SR Ca2+ handling proteins, thereby preventing the development of cardiac remodeling after MI. The gene discussed is GCH1; the disease is myocardial infarction.