A time-dependent decrease of I-κB-α protein was demonstrated in the presence of RANK-L or TNF-α (Figure 5), confirming that the stimulation of cell surface RANK in neutrophils pretreated with SF from patients with RA was followed by intracellular signaling through, at least in part, the NF-κB pathway. Here, TNFRSF11A is linked to rheumatoid arthritis.