Interestingly, a recent study performed by Guo et al. [17] shows that the continuous administration of soluble recombinant IL-23 receptor (IL-23R) cytokine-binding homology region blocks the interaction between IL-23 and the IL-23R and ameliorates the clinical signs of EAE, paving the way for similar strategies, such as secukinumab (anti-IL-17A antibody), to treat Th17-mediated autoimmune diseases, including MS [18]. The gene discussed is IL23R; the disease is autoimmune disease.