Additionally, mice with macrophage-specific activation of YAP develop higher levels of cardiac fibrosis and reduced cardiac function following myocardial infarction, compared to wild-type control mice, suggesting that YAP activation in macrophages contributes to increased fibrosis and accumulation of ECM proteins, consequently leading to worsened outcomes following myocardial infarction (Mia et al., 2020). This evidence concerns the gene YAP1 and myocardial infarction.