The metabolic profiling of T cell subsets also reveals their dependency on glycolysis or OXPHOS. The enzyme pyruvate dehydrogenase (PDH) has been found as a central node in the programming of T cells to use either glycolytic or oxidative metabolism for their differentiation. Indeed, pyruvate metabolism plays a crucial role in Teffs and Tregs conversion. The enzymatic activity of PDH is inhibited by PDH kinases (PDHKs). PDHKs are highly expressed on Th17 cells, but not on Th1 cells and at low levels in Tregs under the influence of hypoxia inducible factor 1- α (HIF1-α) [2, 58-60]. Inhibiting PDHK1 with specific inhibitors such as dichloroacetate (Table 1), which promotes oxidative phosphorylation selectively suppresses Th17 cells therefore favors Tregs generation [61]. This suppression causes the production of reactive oxygen species (ROS), and treating with ROS scavengers such as N-acetyl cysteine (NAC) restore Th17 cell generation [2].