Even as enantiomers, S-2-hydroxyglutarate treatment significantly increases the in vivo proliferation, persistence and antitumor activity of adoptively transferred CD8+ T cells [81], while tumor-derived R-2-hydroxyglutarate induces a perturbation in nuclear factor of activated T cell transcriptional activity and polyamine biosynthesis, leading to the suppression of T cell activity [82]. The gene discussed is CD8A; the disease is neoplasm.