Although synovial fibroblasts are the primary source of CCL13 in the context of RA, several studies have demonstrated that CCL13 can be produced in response to different stimuli by other types of fibroblasts, such as dermal fibroblasts, colonic subepithelial myofibroblasts, and nasal polyp fibroblasts (51–53). This evidence concerns the gene CCL13 and nasal cavity polyp.