Meanwhile, the decreased p53 levels and increased VEGF-A/B expressions in VNS-treated MI-hearts were observed, accompanied by attenuated cardiac hypertrophy, in accord with the results that overexpression of VEGF-A or VEGF-B in myocardium did not promote cardiac hypertrophy39, or only induced physiological hypertrophy21, while contributing to neovascularization. The gene discussed is TP53; the disease is myocardial infarction.