The hypermethylated T-ALL phenotype (~ 25% of all T-ALL patients) is frequently associated with promoter methylation and transcriptional silencing of the tumour suppressor gene and DNA demethylating enzyme, TET2. Notably, re-expression of TET2 through HMA treatment resulted in increased cell death in T-ALL cells, suggesting that targeting DNA methylation may be particularly beneficial in TET2-silenced T-ALL [5–7]. The gene discussed is TET2; the disease is acute lymphoblastic leukemia.