Blocking the actions of Ang II either with AT1R blockers or ACE inhibitors is an accepted treatment strategy to reduce adverse cardiac remodeling following myocardial infarction, but it may entail unfavorable effects such as the paradoxical activation of a negative feedback loop within the Renin–Angiotensin cascade, leading to systemic elevation of Ang II [28,29,30]. Here, AGT is linked to myocardial infarction.