A very rapid series of elegant studies have shown i) that IDH1/2 and TET2 mutations are mutually exclusive in myeloid malignancies [68], ii) that mutated IDH1 and IDH2 produce 2-hydroxyglutarate instead of alpha-ketoglutarate (αKG) [69,70], iii) that TET2 encodes an αKG–dependent methyl cytosine dioxygenase whose mutation alters the conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) [68,71] and iv) that both IDH1/2 and TET2 mutations impact on DNA methylation and are involved in the same biochemical pathway [72]. This evidence concerns the gene IDH1 and myeloid neoplasm.