S100A4 could act as damage-associated molecular pattern once secreted by the action of specific chemokines, stress or necrosis.[38] Related studies found that S100A4 had an elevated levels in several inflammatory diseases such as arthritis, kidney fibrosis and neuronal injury.[39,40] In chondrocytes, stimulation of T cells with S100A4 was proved to have an increased production of cytokines, especially eotaxin-2 and granulocyte colony-stimulating factor, both of which are important factors in the pathogenesis of asthma. This evidence concerns the gene S100A4 and arthritic joint disease.