As expected, after MI in adult mice, knockdown of YAP1 inhibited cardiomyocyte proliferation, promoted apoptosis, and exacerbated myocardial fibrosis resulting in severely impaired cardiac function; in vitro, overexpression of YAP1 induced cardiomyocyte proliferation and reversed H2O2-induced cell death [130]. Here, YAP1 is linked to Myocardial fibrosis.