Indeed, our study confirmed that AF transformation and migration involved in AAA lesions, which may be facilitated by YAP1; in vivo study showed that YAP1 inhibitor‐Verteporfin diminished AF transformation to myofibroblast and migration; in vitro study proved furtherly that YAP1 inhibitor‐verteporfin remarkably attenuated the process of AF transformed to myofibroblast by inhibiting α‐SMA expression and migration demonstrated by wound healing experiment. Here, ACTA1 is linked to triple-A syndrome.