Given the markedly increased levels of CCL3, TNF, and Dkk3 in RA SBM B cells, all of which can inhibit OBs22–24, we next examined for changes of signaling pathways in MPCs downstream of these factors (CCL3 activates ERK signaling25, TNF activates NF-κB signaling26, and Dkk3 inhibits β-catenin signaling27). This evidence concerns the gene CCL3 and rheumatoid arthritis.