Considering our mRNA microarray analysis showing a 3.2-fold increase of β-arrestin2 expression in Ang II–injured aortas from smcKlf5−/− mice relative to that from wild-type (WT) mice, and that Klf5 deficiency in VSMCs facilitated β-arrestin2 expression (S3C Fig), it is reasonable to conclude that Klf5 down-regulation at the late stage of mouse AAA could lead to β-arrestin2 up-regulation through an as yet unidentified mechanism. The gene discussed is AGT; the disease is triple-A syndrome.