Here, we showed that a novel FPR2 agonist (scolopendrasin IX) elicited strong therapeutic effects against the K/BxN serum-transfer arthritis model (Fig. 4), which was blocked by an FPR2 antagonist (WRW4) (Fig. 6), suggesting that stimulation of FPR2 resulted in therapeutic activity against RA. This evidence concerns the gene FPR2 and arthritic joint disease.