Notably, CATH-1 dose-dependently upregulated the secretion of IL-1β when CATH-1 was incubated with cells at post-infection, which is similar to CATH-2 which promotes NLRP3 inflammasome activation, leading to IL-1β secretion [23, 37], suggesting the possibility that CATH-1 serves as a second signal activating inflammasome. The gene discussed is IL1B; the disease is infection.