Moreover, we have demonstrated for the first time that the downregulation of cPLA2 protein/mRNA by CORM-2 could be mediated by the reduction in NF-κB transcriptional activity which would be dependent on the inhibition of IKKα/β phosphorylation leading to attenuation of nuclear translocation of NF-κB. These results elucidate the molecular mechanisms underlying the pharmacological effects of CORM-2 and may lead to the development of novel therapeutic strategies of RA. Here, PLA2G4A is linked to rheumatoid arthritis.