Evidence indicates that CD209 is implicated in autoimmune pathways related to RA, facilitating the differentiation of follicular T helper cells and enhancing interleukin (IL)-27 production, which subsequently exacerbates joint inflammation and injury by activating fibroblast-like synoviocytes (FLSs), key effector cells in RA pathogenesis.[20] Prior research indicates that SNPs in the CD209 gene may influencee the severity of RA,[21] although their correlation with RA susceptibility has not been explored in Egypt. This evidence concerns the gene CD209 and rheumatoid arthritis.