The mIDH1 enzyme produces (R)-2-hydroxyglutarate, which in turn supports the maintenance of cholangiocarcinoma tumors with an immune evasion program centered on a dual mechanism mediated by (R)-2-hydroxyglutarate (suppression of CD8+ T cell activity and tumor cell-autonomous inactivation of TET2 DNA demethylase) (76, 77). This evidence concerns the gene CD8A and neoplasm.