In effect, bone erosions in arthritis result from the combination of multiple signals that include high levels of RANKL in FLS, B, and T cells (34); the inflammatory cytokines TNFα, IL-1, and IL-6, both in RANKL dependent and independent pathways (34–36); and anti-CCP and other RA autoantibodies (37). The gene discussed is IL1B; the disease is arthritic joint disease.