There is now a growing consensus that impaired metabolic rewiring of T cells is central to the pathogenesis of SLE. It could be argued that the most well-documented metabolic impairment in SLE T cells, especially in human patients, are differences in mitochondrial utilization of glucose. When stimulated, SLE T cells show a marked increase in glycolysis and OXPHOS 10 with potentially lowered NADPH production through the PPP . SLE T cells are characterized by a high oxidative state and depleted levels of glutathione .