A deficiency or inhibition of TNF-α was reported to limit AAA severity by multiple mechanisms in these studies, including reducing pro-inflammatory cytokines and adhesion molecule expression, limiting macrophage infiltration and reducing vascular endothelial growth factor (VEGF-A) expression, neoangiogenesis, matrix metalloproteinase (MMP) activity and extracellular matrix (ECM) remodeling (Table 2) [28,29]. This evidence concerns the gene TNF and triple-A syndrome.