Ang (1–7) exerts potent vasodilatory, anti-inflammatory, and anti-proliferative effects by binding to MasR and the angiotensin type 2 receptor (AT2R) [26,27,28]; thus, this ACE2-induced shift in the ‘balance of power’ from Ang II to Ang (1–7) prevents post-stroke vasoconstriction and the pro-thrombotic and vascular inflammatory phenotype (Figure 2). This evidence concerns the gene MAS1L and Stroke.