Consistently with these data, we found that, in RRMS patients, CD28-mediated up-regulation of Th17 cytokines (Figure S2) was associated to an increase of the glycolytic program (Figure 2a–c) and was strongly impaired by 2-DG glycolysis inhibitor (Figure 2g–l). The gene discussed is CD28; the disease is relapsing-remitting multiple sclerosis.