Gene-expression analyses have shown that genes that were downregulated after IL-1β inhibition in sJIA patients were conversely found to be upregulated in AOSD patients.29,30 These genes (e.g. IL-1β, IL-1 receptor accessory protein, IL-1 receptor antagonist protein, IL-1receptor, type I and IL-1 receptor, type II) that are upregulated in AOSD are all involved in IL-1 signalling pathways, indicating that AOSD is an IL-1–driven condition, mechanistically similar to sJIA. This evidence concerns the gene IL1A and adult-onset Still disease.