This may translate to RA, in the example of anti-TNF combination treatments, as patients with a “lymphoid” phenotype (synovium dominated by B cells and plasmablasts) and with high baseline serum levels of the B-cell chemoattractant CXCL13 showed greater resistance to anti-TNF treatment than patients with RA with a “myeloid” phenotype (synovium rich in inflammatory macrophages) [43]. This evidence concerns the gene CXCL13 and rheumatoid arthritis.