Furthermore, our laboratories have demonstrated that in vivo inhibition of NF-κB activation in a pre-clinical arthritis model is associated with decreased NF-κB-induced cytokines or NF-κB-mediated tissue destructive processes (i.e., formation of bone-resorbing osteoclasts) known to be closely linked with adverse clinical outcome (Figure 1) (14–16). The gene discussed is NFKB1; the disease is arthritic joint disease.