Inactivation of transforming growth factor β (TGF‐β) cascade accelerates the development and rupture of AAA via the inhibition of ECM synthesis and promotion of matrix degradation.5, 6 Prolyl‐4‐hydroxylase α1 (P4Hα1) is the rate‐limiting factor of P4H enzyme, which is regulated by TGF‐β1, and is the key enzyme for collagen synthesis.7 In addition, inflammatory response also has an imperative role in the advancement of AAA. Here, TGFB1 is linked to triple-A syndrome.