In addition, high level DCA also significantly up-regulated molecules related to the pathogenicity of Th17 cells, such as CCR6, a chemokine receptor crucial for pro-inflammatory function of Th17 in autoimmune disease involving EAE and arthritis, and GM-CSF as well as GZMB, the critical components of pathogenic Th17 signature [22–24] (Fig. 1c). This evidence concerns the gene CSF2 and Arthritis.