Moreover, a recent study showed that TRAF1’s ability to negatively regulate the linear ubiquitination of ASC is crucial for controlling inflammasome activation and that TRAF1-deficient mice exhibited exacerbated inflammation and joint swelling in the MSU crystal–induced arthritis model, an NLRP3 inflammasome–dependent model of gout, compared to WT littermates.4 This evidence concerns the gene TRAF1 and arthritic joint disease.