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. This evidence concerns the gene SENP3 and triple-A syndrome.