The YAP/TAZ can promote the proinflammatory response by increasing the expression of IL-6 and reducing the expression of arginase 1(Arg1) by interacting with the histone deacetylase 3 (HDAC3)—nuclear receptor corepressor 1 (NCoR1), thereby enhancing MI-induced cardiac fibrosis and remodeling. Here, YAP1 is linked to myocardial infarction.