AIM2 and neoplasm: Another study highlights that low-dose chemotherapy preferentially leads to DNA damage and the accumulation of cytosolic dsDNA in ileal epithelial cells, able to activate the AIM2 inflammasome signaling to trigger cell–cell crosstalk in the small intestine [16]; specifically, the authors found that AIM2-dependent IL-18 release led to the interplay between proximal Th1 and Paneth cells in ileal crypts responsible of the impairment of antimicrobial functions of proximal Paneth cells and the ensuing ileal microbiome changes associated with anti-tumor immune response [16].