Previous studies have reported that STUB1/CHIP, an essential E3 ubiquitin ligase, facilitates the degradation of SENP3 under non‐stress conditions in tumor cells.[13] Recently, STUB1/CHIP has been implicated in the pathogenesis of atherosclerosis via control of SIRT6 stability in VSMCs.[14] To explore the molecular mechanism by which SENP3 expression is regulated in AAA, we interrogated the expression profile of STUB1 in macrophages in AAA. Here, SIRT6 is linked to triple-A syndrome.