Our research group found that AIM2 is highly expressed in circulating cells collected by exacerbated COPD patients and that its stimulation via Poly dA:dT induced the release of IL-1α in a canonical, caspase-1-dependent, and non-canonical, caspase-4-dependent manner, which in turn, was responsible for the release of the immunosuppressive and pro-fibrotic cytokine TGF-β [13,95]. Here, AIM2 is linked to chronic obstructive pulmonary disease.