In a murine DCM model, endogenous Angiotensin II (Ang II) was shown to activate YAP1 and promote the proliferation of cardiac fibroblasts and their transdifferentiation to myofibroblasts; subsequently, these changes were found to induce cardiac remodeling and impaired cardiac contractility (Jin et al., 2019). This evidence concerns the gene AGT and familial dilated cardiomyopathy.