Our results indicate a previously unrecognised role for inflammatory pathways in some mAIDs, such as JAK–STAT signalling in TRAPS, and the production of Th17-related cytokines that pave the way for the study of other noncanonical autoinflammatory pathways and the role of Th17 cells in autoinflammatory diseases. The gene discussed is SOAT1; the disease is TNF receptor 1-associated periodic fever syndrome.