In vivo studies in mice have shown that under cell stress conditions such as starvation or myocardial ischemia/reperfusion, it can accelerate the dephosphorylation of FoxO1, and increase the nuclear transcription activity of FoxO1 transcription factors, increase the level of cardiac autophagy, and reduce cardiomyocyte hypertrophy (Sengupta et al., 2009). The gene discussed is FOXO1; the disease is myocardial ischemia.