STAT1 and myeloid sarcoma: Primarily, IL-27 was proposed to provoke pro-inflammatory state by meliorating T-helper 1 (Th1) differentiation from naïve T cells in early immune response via Signal Transducer and Activator of Transcription 1 (STAT1) [7–9]; however, subsequent work using human and animal models of MS have indicated that IL-27 has considerable inhibitory influences on Th1, Th2, and Th17 (IL-17A and IL-17F) subsets of T cells, and on Antigen-Presenting Cells (APCs) function.