An expanding body of evidence underscores the role of various cellular effectors and signaling pathways in hypertension, as well as Ang II-induced cardiac fibrosis,[37,38] oxidative stress,[39,40] and inflammation.[41] The complexity of signaling pathways, profibrotic mechanisms, and types of fibrosis indicates that a “one-size-fits-all” approach is unlikely to be effective for all heart diseases associated with fibrosis.[42] Consequently, researchers are anticipated to continue exploring therapeutic targets and strategies for the treatment of MF. Here, AGT is linked to hypertensive disorder.