NF-κB activation [12] as well as increased TLRs [13] and NLRP3 [14] expression can be detected in synovial tissue from RA patients, but several other molecules activating the pathway (TNF-α, IL-1β) [15] or regulated by the pathway, e.g. IL-17 [15], are central in the pathogenesis of RA. This evidence concerns the gene NLRP3 and rheumatoid arthritis.