Our clinical-molecular-immunologic analyses of a large number of samples from patients with arthritis-irAE revealed (1) a prominent IFNγ-producing T cells in SF; (2) expansion of SF Tregs with heightened suppressor functions; (3) potential role of effector CD8+ T cells; and (4) enhanced Th17 cell signatures in combined ICI arthritis with steroid resistance (Fig. 7). The gene discussed is IFNG; the disease is arthritic joint disease.