As one result, HIF-1α shifts the balance from Tregs to effector Th17 cells by (i) promotion of glycolysis [200] but also (ii) by binding of the Treg-specific transcription factor Foxp3 and its subsequent degradation favoring pro-inflammatory effector Th17 cells which drive inflammation and can lead to autoimmunity [199,200]. This evidence concerns the gene HIF1A and Autoimmunity.