Those findings are highly significant, given recently described SNPs in the A20/TNFAIP3 locus, imparting decreased A20 expression or function (NFκB inhibition), that were linked with auto-immune and pro-inflammatory pathologies such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis [82,83]. This evidence concerns the gene TNFAIP3 and rheumatoid arthritis.