According to the hypothesis that the balance between apoptosis and proliferation of VSMCs was destroyed in aortic diseases (Figure1a), we determined the AIP alternation in human thoracic AD and AAA tissues (Participants' basic information is shown in Table S1, Supporting Information) and in mouse models of AD and AAA by immunofluorescence staining of VSMC marker (smooth muscle α‐actin, SMA), Ki‐67, and TUNEL. Here, MKI67 is linked to triple-A syndrome.