ILCs with a similar phenotype were also present in normal joints and expanded in collagen antibody-induced arthritis in C57/BL6 mice, indicating that the presence and expansion of GM-CSF-producing synovial ILCs was not dependent on the mouse genetic background or the mode of arthritis induction by autoimmune Th17 cells or autoantibody (Figures 4K and S4). Here, CSF2 is linked to Arthritis.