Taken together, our results demonstrated that ZFP36 manipulated VSMC phenotypic switch via regulating GBP2/YAP1/TEAD1 signaling; ZFP36 knockdown promoted GBP2 expression and TEAD1 degradation, which led to YAP1 dissociating from TEAD1 and bonding to KLF4, forming the YAP1/KLF4 complex and causing VSMC phenotypic switch and AAA progression. Here, ZFP36 is linked to triple-A syndrome.