As a crucial molecule for myocardial angiogenesis, VEGF expression was usually regulated by Hif-1 under hypertrophic stimuli or hypoxia/ischemia, and the series of events were terminated by p53 accumulation, causing the disruption of coordinated cardiac hypertrophy and angiogenesis, driving the transition to HF in pressure overload model except for LAD-induced MI model6–11. The gene discussed is TP53; the disease is hypertrophy.