As T-ALL has (i) a uniquely hypermethylated phenotype among all cancers [6], (ii) the hypermethylation phenotype is associated with TET2 silencing [5], and (iii) TET2 expression can be rescued with AZA [5], we investigated the potential of pharmacological removal of DNA methylation in T-ALL cell lines as an avenue for therapeutic action. The gene discussed is TET2; the disease is cancer.