In animal models of AAA, B cell defects have beenshown to inhibit AAA formation and progression, which may be related to adecrease in spleen tyrosine kinase (Syk) activation and MMP-9 expression [67], or due to an increase inplasma cell like dendritic cells (DCs), resulting in an increase in Tregs and adecrease pro-inflammatory factors [68]. This evidence concerns the gene MMP9 and triple-A syndrome.