This review illustrates the potential of kallistatin in suppressing AAA development through attenuating a wide range of pathological mechanisms (Figure 4) including VEGF induced angiogenesis and inflammation, oxidative stress induced angiogenesis and apoptosis, TNF-α induced inflammation, apoptosis and MMPs production, as well as Wnt canonical signaling induced angiogenesis and inflammation. This evidence concerns the gene VEGFA and triple-A syndrome.