['Many patients with rheumatoid arthritis (RA) benefit from tumor necrosis factor-α blocking treatment (anti-TNF), but about one third do not respond. The objective of this study was to replicate and extend previously found associations between anti-TNF treatment response and genetic variation in the TNF-, NF-κB- and pattern recognition receptor signalling pathways.', 'Forty-one single nucleotide polymorphisms (SNPs), including 34 functional, in 28 genes involved in inflammatory pathways were assessed in 538 anti-TNF naive Danish RA patients with clinical data. Multivariable logistic regression analyses were performed to test associations between genotypes and treatment response at 3-6 months using the European League Against Rheumatism (EULAR) response criterion. American College of Rheumatology treatment response (ACR50) and relative change in 28-joint disease activity score (relDAS28) were used as secondary outcomes. Subgroup analyses were stratified according to smoking status, type of anti-TNF drug and IgM-Rheumatoid Factor (IgM-RF) status. False discovery rate (FDR) controlling was used to adjust for multiple testing.', 'Statistically significant associations with EULAR response were found for two SNPs in NLRP3(rs4612666) (OR (odds ratio) for good/moderate response\u200a=\u200a0.64 (95% confidence interval: 0.44-0.95), p\u200a=\u200a0.025, q\u200a=\u200a0.95) and INFG(rs2430561) (OR\u200a=\u200a0.40 (0.21-0.76), p\u200a=\u200a0.005, q\u200a=\u200a0.18) and among IgM-RF positive patients for TNFRS1A(rs4149570) (0.59 (0.36-0.98), p\u200a=\u200a0.040, q\u200a=\u200a0.76). Current smokers who carried the NLRP3(rs4612666) variant allele were less likely to benefit from anti-TNF treatment (OR\u200a=\u200a0.24 (0.10-0.56), p\u200a=\u200a0.001, q\u200a=\u200a0.04).'] Is anti-TNF treatment response in rheumatoid arthritis patients associated with genetic variation in the NLRP3-inflammasome?