The discordance between a high level of anti-inflammatory RBPs and the presence of chronic inflammation in LN patients makes us think about the failure of the mode of action of these RBPs and leads us to believe that these RBPs can be phosphorylated or inhibited by pro-inflammatory RBPs, in particular AT-rich interactive domain-containing protein 5A (Arid5a), following competition for the same protein binding site, thus facilitating the initiation and efficiency of inflammatory mediator production. This evidence concerns the gene ARID5A and inflammation.