Cross-mining of these data with genes already implicated in the (SF) pathogenesis of RA (S1 Table) further supports the hypothesis that ES-62 does not simply prevent remodelling of SFs during CIA: rather, this analysis suggests that by (additionally) modulating expression of genes (e.g. miR146, Lair1, Pak1, Pik3ca, Map1lc3b, Aspn, Ccl25, Mmp12, Spag16 and Adipoq) implicated in the dysregulation of SF responses, ES-62 may stably rewire CIA-SFs to a distinct and protective “resolving” phenotype that may counter developing and established inflammation and bone destruction in the joint. This evidence concerns the gene CCL25 and rheumatoid arthritis.