AGTR1 and triple-A syndrome: Moreover, at least two different biased signals, Gq and β-arrestin pathways, have recently been shown to mediate distinct AT1 functions.10,49,57,58 These observations led to two tightly associated and important unanswered questions regarding the role of AT1 signaling complexes in vascular homeostasis and disease states, which are: (1) how is endogenous AT1-biased signaling fine-tuned in healthy vessels to maintain cardiovascular homeostasis, and (2) what is the mechanism underlying the dysregulation of AT1-biased signaling associated with vascular pathogenesis, such as AAA formation?