IL-1β and IL-18 play a central role in AOSD pathophysiology and further promote immune cells to produce a large amount of pro-inflammatory cytokines, including IL-6, IL-8, IL-17, and tumor necrosis factor (TNF)-α, type I interferons (IFN-α and IFN-β), as well as IL-1β and IL-18 themselves, leading to an amplified inflammatory response. This evidence concerns the gene IL6 and adult-onset Still disease.