Studies using autologous cellular debris (CD) from late-stage AAA tissues to stimulate VSMCs revealed strong NF-κB activation, the activation and release of inflammasomes such as AIM2 and NLRP3, and the secretion of various pro-inflammatory factors, highlighting the crucial role of NF-κB in AAA-related inflammation in VSMCs [76]. This evidence concerns the gene NFKB1 and triple-A syndrome.