Specifically, we demonstrated that BAF60c is required to recruit the SWI/SNF complex to the BCL2 promoter and subsequently engage in a regulatory interaction with KLF5 to activate BCL2 expression in VSMCs, thus uncovering a BAF60c-dependent antiapoptotic regulation to prevent VSMC loss during AAA development. This evidence concerns the gene SMARCD3 and triple-A syndrome.