T cell glycolysis and mitochondrial metabolism as potential therapeutic targets are supported by elevated glycolytic metabolism in T cells of systemic lupus erythematosus (SLE) patients and reduced IFN-γ production and disease biomarkers upon inhibition of CD4+ T cell glycolysis in mouse models of SLE (Yin et al., 2015). Here, IFNG is linked to systemic lupus erythematosus.