By contrast, Nfat5-haplodeficient and Tlr2/4-deficient mice all exhibited a milder form of SAA-accelerated arthritis, including synovial hyperplasia and bone damage, which was accompanied by diminished macrophage infiltration, thereby confirming the critical role of SAA-TLR2/4-NFAT5 axis in macrophage migration and chronic arthritis in vivo. This evidence concerns the gene SAA2 and arthritic joint disease.