In RA CD4 T cells, glucose is shunted from glycolytic breakdown towards the pentose phosphate pathway (PPP). Transcriptional repression of phosphofructokinase/fructose biphosphatase 3 (PFKFB3) results in reduced ATP and pyruvate production. Upregulation of Glucose-6-phosphate dehydrogenase (G6PD) funnels glucose towards the PPP, supplying NADPH, reduced glutathione (GSH) and biosynthetic precursors. As an outcome, the cell’s redox status shifts towards reductive stress, impairing redox-dependent signaling. Also, the cell has access to biosynthetic precursors, enabling a cell building program.