In the context of developing biologics for the suppression or treatment of EAE or MS, it is of note that STAT1 and STAT3 play critical roles in the development of Th1 and Th17 subsets, respectively, and they also regulate the initiation, duration and intensity of proinflammatory immune responses that mediate EAE [2,3]. This evidence concerns the gene STAT3 and myeloid sarcoma.