Bulua et al., using mouse embryonic fibroblasts expressing different mutations of the type 1 TNF receptor (TNFR1) associated with the autoinflammatory disorder tumor necrosis factor receptorassociated periodic syndrome (TRAPS), found that TNFR1 mutant cells have elevated basal levels of mitochondrial ROS, and this mitochondrial ROS is important for lipopolysaccharide-stimulated production of the proinflammatory cytokines IL-6 and TNF, but not IL-1β, in the absence of inflammasome formation. Here, TNFRSF1A is linked to TNF receptor 1-associated periodic fever syndrome.