In the 4T1 and B16F10 mouse tumor models, our results further suggest that low levels of cancer cell pyroptosis activated the secretion of proinflammatory cytokines (such as TNF-α, IFN-γ, IL-1β, and IL-18), upregulated the expression of DAMPs, recruited the infiltration of various immune cells, and inhibited the growth of established tumors, thereby establishing a positive feedback loop to promote antitumor immunity. The gene discussed is IL1B; the disease is neoplasm.