Interestingly, recent studies postulate an anti-tumour effect of 2-HG, whereby 2-HG inhibition of FTO, the primary enzyme responsible for m6A demethylation, promotes transcriptional and metabolic changes that underpin the survival advantage that mutant-IDH glioma patients have relative to wild-type IDH patients [58,67–69], although this survival trend appears to be debatable in AML [70–73]. The gene discussed is IDH1; the disease is neoplasm.