To clarify whether the down-regulation of Klf5 expression at the late stage of the AAA is an effect of desensitization of the Ang II receptor, we performed western blot analysis to detect extracellular signal–regulated kinase 1/2 (ERK1/2) signaling, which is one of signal pathways activated by Ang II binding to the AT1 receptor, and the expression of β-arrestin2 that mediates desensitization of G protein–coupled receptors (GPCRs) in Ang II–induced mouse AAA models. Here, AGTR1 is linked to triple-A syndrome.