Usui et al. found that TXNIP-NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation by mitochondrial oxidative stress in macrophages leads to the development of AAA, while the inhibition of NLRP3 can inhibit aneurysmal formation, arterial dilation rate, and inflammatory cell infiltration of ApoE−/− mice induced by angiotensin II (Ang II) [10]. The gene discussed is AGT; the disease is triple-A syndrome.