Although Hif1α-deficient T cells have better cellular growth and proliferation in response to TCR engagement with IL-3 (76), HIF1α–mediated metabolic reprogramming toward ‘aerobic glycolysis’ (76, 77) promotes Th17 cell differentiation and declines Treg cell differentiation in both in vitro experiment, and in vivo animal model of MS (77, 78) (Figure 3A). This evidence concerns the gene HIF1A and myeloid sarcoma.