Despite considerable insight in the epigenetic alterations resulting from the gain‐of‐function mutation in IDH1 or IDH2, the metabolic consequences of the mutant enzyme, whether D2HD‐dependent or not, are still poorly understood, in part due to the difficulties in establishing IDH‐mutant gliomas in culture and/or in vivo as xenografts. The gene discussed is IDH2; the disease is central nervous system cancer.