In terms of other disease risks, rheumatoid arthritis-associated single nucleotide polymorphisms have been described in PKCθ, which lies upstream of TCR-induced IκB degradation, in c-Rel, and in c-Rel target genes CD40 and TNFAIP3 [57], [58], [59]; and IκBε itself is upregulated at the mRNA level by TNF, whose over-expression is a feature of rheumatoid arthritis and other inflammatory diseases [52]. This evidence concerns the gene TNFAIP3 and rheumatoid arthritis.