Wang et al. (2021) showed that Ang II stimulation of AT1R could induce M1 macrophage polarization and macrophage infiltration via stimulating the YAP pathway, and blockade of AT1R by ARB could reduce aortic inflammation and aortic dissection incidence. Zhang et al. (2014) reported somewhat opposite effects that depletion of macrophage AT1A receptor (a subtype of AT1R) heightened M1 macrophage proinflammatory cytokines and exacerbated renal fibrosis induced by unilateral ureteral obstruction. Here, AGTR1 is linked to Aortic dissection.