Consistent with previous studies, we found AF transformation contributed to AAA development, and YAP1 activated AF phenotype transformation and migration, which were remarkably blocked by YAP1 inhibition through YAP1 inhibitor‐Verteporfin; more critically, intraperitoneal injection of Verteporfin significantly attenuated collagen deposition, alleviated AAA development, reduced AAA incidence, Verteporfin might be a very promising clinical drug for AAA therapy. The gene discussed is YAP1; the disease is triple-A syndrome.