For instance, levels of both IL-17 and IL-6 were shown to positively correlate with neurological disabilities in MS patients (18), and blockade of IL-6-dependent pathways using an anti-IL-6 receptor antibody limited the development of EAE in mouse models, most likely by counteracting the differentiation and expansion of pathogenic TH17 cells while promoting Treg cell responses (54, 55). This evidence concerns the gene IL17A and myeloid sarcoma.