The inhibitory effect on arthritis was not linked to any of the known ACPA clones’ fine-specificities, nor to a previously reported histone epitope associated with this effect (online supplemental figure 1E).2 The anti-inflammatory effects induced by mC03 were clearly FcγR-dependent, with both its F(ab’)2 fragments and FcγR null (GRLR-mutated) variants incapable of suppressing arthritis development (figure 1G, H; comparison between murine and human C03 ACPA in online supplemental figure 2D). This evidence concerns the gene PRTN3 and arthritic joint disease.