In addition to an essential role for Th22 and Th17 in MS, these data suggested that the two Teff types may play synergistic roles in disease progression and yielded speculation that since IL-23 promotes IL-17 and IL-22 secretion, IL-23 receptor and STAT3 signaling may provide a key pathway in the activation of Th22 cells and Th17 Teffs. This evidence concerns the gene IL17A and myeloid sarcoma.