Moreover, using a mouse model of cigarette smoking-induced COPD, we demonstrated that smoking exposure led to the release of inflammasome-associated IL-1-like cytokines (IL-1α, IL-1β, IL-33, IL-18) and increased the expression of AIM2 in lung-recruited macrophages in wild type C57Bl/6 mice, but not in 129Sv mice, who lack a functional caspase-11, the murine analog of human caspase-4 [96,97,98]. The gene discussed is AIM2; the disease is chronic obstructive pulmonary disease.