Within RA pathogenesis, IL-23 secretion by activated dendritic cells and macrophages initiates a pathogenic cascade wherein cytokine binding to IL-23 receptors on Th17 cells triggers JAK2-mediated phosphorylation of the receptor complex, facilitating STAT docking site formation and nuclear translocation of phosphorylated STAT dimers (Bridgewood et al., 2020); this not only amplifies Th17 proliferation and survival but drives their differentiation into CCR6-expressing pathogenic Th17 subsets (pTh17), which secrete copious IL-17A/F and GM-CSF (Parween et al., 2025). This evidence concerns the gene IL17A and rheumatoid arthritis.