as well as those in SLE patients. Unfortunately, even the most basic quantification of differences in metabolic demands is not available. For example, it is well established that SLE T cells have higher mitochondrial mass . But systematic changes in organelle distribution and their effect on overall biomass composition in SLE are not known. Similarly, the cytokine secretion profile is significantly altered between SLE and healthy T cells , with an increased production of pro-inflammatory cytokines in SLE. However, the metabolic burden of increased cytokine production by SLE T cells has not been quantified. Altered metabolic demands related to biomass and cytokine production have a direct effect on the nutrient uptake profile, downstream nutrient usage, and consequently the entire metabolic network. For example, increased protein (cytokine) production requires higher levels of synthesis of amino acids and higher ATP demand . Similarly, increased organelle mass requires higher de novo lipid synthesis, which in turn requires increased NADPH and NAD+ 44 regeneration rates. Therefore, to elucidate metabolic driving mechanism of SLE pathogenesis and to discover new druggable targets for SLE and other autoimmune disorders, we need a systematic and unbiased characterization of the differences in metabolic requirements as well as metabolic network activity of SLE and healthy T cells.