To better understand the role of IL-6 signaling in AAA pathogenesis at the cellular level, we examined the nuclear localization of NFκB, a mediator of AAA pathogenesis [6], pStat3, a mediator of IL-6 signaling, and pSmad2, a mediator of TGFβ signaling that is involved in inflammation, ECM metabolism, and regulation of smooth muscle cell function [24], together with staining for smooth muscle α-actin (SMA), a marker of smooth muscle cells (SMCs) (Fig 6A). This evidence concerns the gene NFKB1 and triple-A syndrome.