Utilizing AIM2−/− mice in a diethylnitrosamine-induced hepatocellular carcinoma model, research has demonstrated that AIM2 inflammasome activation in Kupffer cells promotes inflammation-associated tumor initiation in the liver; conversely, AIM2 deficiency diminishes hepatocellular carcinoma development in these mice.549 In contrast, studies employing mouse models of sarcomas, which are highly immunogenic, and melanoma, which is relatively non-immunogenic, have shown that STING activation in innate immune cells, including myeloid cells and DCs, inhibits tumorigenesis. Here, AIM2 is linked to neoplasm.