In FLS, TNF-α-activates Syk/PKC-d/JNK/c-Jun pathway to induce IL-32 (isoforms α, β, δ, and γ) [127], suggesting a splicing of IL-32γ into IL-32β [110]; interestingly, IL-32β is associated with lower inflammation and less severity of RA when compared with IL-32γ. This evidence concerns the gene TNF and rheumatoid arthritis.