IMMUNOMETABOISM AS A THERAPEUTIC TARGET IN TRANSPLANTATION: Organ transplantation is the last therapeutic approach used to treat end-stage organ failure. Current therapeutic approaches for organ rejection target overall immune suppression, which is associated with severe side effects, cancer, and mortality. However, targeting a more specific immune suppression has become more favorable in clinical settings to treat transplant rejection. The long term survival of transplanted graft is limited by surgical trauma and ischemaic reperfusion injury (IRI). These unavoidable events trigger innate immune cell activation that eventually promote sterile inflammation. This prolong inflammation causes immunometabolic rewiring especially after ischemia and IRI to fulfill oxgen demand. Ischemia or Hypoxia reduces OXPHOS and hence, induce tissue reliance on aerobic glycolysis [99]. This event enhance the production of pro-inflammatory cytokine that subsequently leads to T cell activation. In fact,the metabolic requirements of Teffs and Tregs and the conclusive role of Teffs/Tregs ratio have been crucial parameters to decide the fate of the transplanted organ. These metabolic requirements could be used as a key tool in specific therapeutic approaches to contain graft associated microvascular injuries and induce specific immune tolerance. In alloimmune inflammation post-transplantation, donor immune cells rely less on lipid metabolism for their energy requirements, whereas the recipient cell depends on aerobic glycolysis [74, 98]. Specifically, CD4+T cell activation in solid organ transplantation more closely resembles the classical metabolic reprogramming that is seen during normal T cell activation [1].