By using in vitro and in vivo glioma models, Bunse and colleagues showed that the glioma cell-derived oncometabolite (R)-2-hydrixyglutarate (R-2HG) is able to suppress CD8+ cell activity by interfering with the calcium-dependent transcriptional activity of nuclear factor of activated T cells (NFAT) and inhibiting T-cell receptor (TCR) signalling [66]. The gene discussed is CD8A; the disease is glioma.