We identified EBF1 as a potential candidate for this role at the transcriptional level through motif analysis of hypermethylated regions in four cancer types where TET function is impaired by increased levels of 2-HG; this hypothesis is supported by proportional enrichment for both EBF1 and TET2 at selected loci establishing co-localisation of the two proteins, and by co-immunoprecipitation of endogenous EBF1 with TET2 which demonstrates their interaction, either directly or indirectly, as part of a larger complex. The gene discussed is EBF1; the disease is cancer.