The persistence of ectopic lymphoid structures in RA synovial tissues following transplantation into SCID mice is likely to be related to the sustained overexpression of genes regulating ectopic lymphoneogenesis and autoreactive B cell survival, such as the TNF family members LTβ, TNFα, and APRIL, as well as the lymphoid chemokine CXCL13 [26,27]. This evidence concerns the gene CXCL13 and rheumatoid arthritis.