Of note, we have since shown that endothelial-specific depletion of MRTF-A was sufficient to dampen angiotensin-II (Ang-II)-induced cardiac hypertrophy in mice (Weng et al., 2015), suggesting that at least part of the mechanism whereby MRTF-A regulates cardiac hypertrophy can be attributed to non-cardiomyocytes. Here, MRTFA is linked to cardiac hypertrophy.