In addition, recent studies have shown that CD4+ TRM cells, particularly TH1 and TH17 subsets, also contribute significantly to RA pathology by driving synovial inflammation, enhancing cytokine secretion (e.g., IFN-γ, IL-17), and promoting tissue damage through immune interactions with fibroblasts and endothelial cells. The gene discussed is IFNG; the disease is rheumatoid arthritis.