Interestingly, USP18-deficient T cells have been demonstrated to be defective in T helper 17 (Th17) cells differentiation and to exhibit hyperactivation of NF-κB and nuclear factor of activated T-cells (NFAT), resulting in an increase in interleukin-2 (IL–2), which suggests the role of USP18 in T cell-mediated adaptive immune response and autoimmune disease. The gene discussed is IL2; the disease is autoimmune disease.