The molecular link between TRAPS and IL-1 is not clear: the pathogenesis may vary with each mutation, but it is possible that IL-1 might act as a proinflammatory mediator downstream of TNF, or that aggregates of misfolded TNF receptors stimulate intracellular signals resulting in enhanced production of IL-1 and other chemokines (44). Here, IL1B is linked to TNF receptor 1-associated periodic fever syndrome.