TET2 mutations in patients are almost always heterozygous (Abdel-Wahab et al., 2009; Delhommeau et al., 2009; Kosmider et al., 2009; Langemeijer et al., 2009), suggesting that enhancing residual TET2 activity, encoded by the remaining wild-type TET2 allele, or restoring the activity of functionally defective mutant TET2 proteins, could be a viable therapeutic strategy for the treatment of patients with AML. Here, TET2 is linked to acute myeloid leukemia.