Given that the production of GM-CSF is induced by IL-23 and dependent on the activity of the IL-12-IL-23 receptor complex and RORγt [45], the reduction of RORγt through blocking the interaction of IL-23 by tIL12rβ1/Fc and the decline of GM-CSF expression in CNS and spleens in this study strongly illustrate the feasibility and therapeutic potential of using tIL12rβ1/Fc for effective treatment of MS and other autoimmune diseases. The gene discussed is IL23R; the disease is myeloid sarcoma.