For example, in 2011, Roberts et al. [42] used a comparative detection of arterial wall samples from 1151 AAA patients and 727 non-AAA patients to establish that NLRP3 homozygous gene rs35829419 and its downstream product IL-1β were significantly overexpressed in the AAA group, suggesting that NLRP3 inflammasome did have a direct or indirect regulatory effect on AAA occurrence. The gene discussed is NLRP3; the disease is triple-A syndrome.