The engaged NLRP3 inflammasome activatescaspase-1, which then converts pro-IL-1β and pro-IL-18 into mature IL-1β and IL-18, join with various cytokines from other pathways, for example, IL-6, IL-8, IL-10, TNF-α, and IFN-γ, to amplify the inflammatory response in a cytokine burst that leads to the onset of AOSD (2, 54–56). This evidence concerns the gene NLRP3 and adult-onset Still disease.