Cellular damage, toxins, and infections can lead to the activation of inflammasome including Toll-like receptor 4 (TLR4) and NLRP3 [19], which recruit caspase-1 and then promote the production of pro-inflammatory cytokines such as IL-1β and IL-18 or activate GSDMD-mediated secondary pyroptosis [43–45] (Figure 7). The gene discussed is IL1B; the disease is infection.