Taken together, clonotypes and trafficking analyses of T cells suggested that SF CXCR3hi CXCR6hi/lo effector CD8+ T cells, recruited via CXCL9/10/11 and CXCL16 secreted by myeloid cells, may contribute to arthritis-irAE disease pathogenesis. The gene discussed is CXCL9; the disease is arthritic joint disease.