The pathophysiological relevance of these findings was confirmed by showing that the application of the glycolysis inhibitor 2-deoxy-D-glucose and of the mitochondrial metabolism inhibitor metformin, were capable to suppress autoimmunity, decrease IFN-γ and IL-17 production and restore IL-2 synthesis, indicating that an altered cellular metabolism contributes to chronic T cell activation in SLE (90, 91). This evidence concerns the gene IFNG and systemic lupus erythematosus.