We also show that promoting HIF-1 function with DFO was able to revert the inhibition of immunometabolic responses and the defective intracellular bacterial control driven by both high-glucose and MGO treatment in control and IFN-γ activated macrophages, constituting a rationale for the design of adjunctive TB therapy in TB/DM comorbidity. This evidence concerns the gene HIF1A and diabetes mellitus.