Moreover, it was reported that adeno-associated virus 9 (AAV9)-YAP1 delivery (the human constitutive active form YAP1S127A) in mouse cardiomyocytes promoted cardiomyocyte division by boosting the cell cycle, as detected by the 4/5-fold higher presence of pHH3 and 5-ethynyl-2 deoxyuridine (EdU) uptake; this was sufficient to reduce scar size and to increase cardiac function in terms of ejection fraction and the attenuation of cardiac remodeling (hypertrophy) after MI, without signs of apoptosis [106]. Here, YAP1 is linked to myocardial infarction.