Importantly the increase of IL-1β is not relevant to its mRNA levels, but corresponding to inflammasome activation which facilitates cleavage of pro-IL-1β.[50] KCs in TAA-treated ALI mice with diabetes mellitus display the trait of NLRP3 inflammasome activation that leads to severer liver injury than TAA-treated ALI mice without diabetes mellitus. The gene discussed is IL1B; the disease is diabetes mellitus.