Hyperglycemia drives increase in glycolysis in activated T cells thus leading to robust IFN-γ production by preventing glycolytic enzyme glyceradehydphosphate dehydrogenase (GAPDH) from binding to and inhibiting the translation of IFN-γ mRNA (2, 74) and thus driving inflammation in a non-antigen specific manner. This evidence concerns the gene IFNG and Hyperglycemia.