To ascertain the pathogenic role of the SAA/NFAT5 axis in vivo, we generated a severe form of SAA-accelerated arthritis by intraarticular administration of SAA (5 μg) into the knee joint of mice with suboptimal severity of IL-1β-induced arthritis, a model of inflammatory arthritis where macrophages play a central role (33). This evidence concerns the gene IL1B and arthritic joint disease.