CD4 T-cell responses to gut microbiota are crucial in regulating intestinal inflammation. Whereas T helper (Th)1 and Th17 cells reactive to gut microbiota are central to the pathogenesis of inflammatory bowel disease (IBD), regulatory T cells (Treg) inhibit it. CD4 T-cell metabolism is highly dynamic. T-cell activation demands biosynthetic precursors and adequate energy for effector function.1 Metabolic reprogramming of T effector cells and Treg cells leads to distinct metabolic programs. If activated T cells fail to induce appropriate metabolic pathways, effector function and the ability to induce or inhibit inflammatory disease are impaired.