In other cases, inhibition of TET function appears to be the underlying cause: for instance in many glioblastomas and myeloid leukaemias, recurrent dominant mutations in IDH1 and IDH2, the cellular enzymes that produce 2-oxoglutarate, result in massively increased levels of 2-hydroxyglutarate55, an ‘oncometabolite' that interferes with the activity of TET enzymes and other dioxygenases56. Here, IDH1 is linked to glioblastoma.