The recent discovery of TET (Ten-eleven-translocation) enzyme functions has led to a paradigm shift in our understanding of how imbalances in DNA methylation-demethylation dynamics are coupled to cancers. The TET proteins (TET1, TET2 and TET3) alter DNA methylation status by sequentially oxidizing 5-methylcytosine. The resulting oxidized methylcytosines function as intermediates in DNA demethylation as well as independent epigenetic marks. Because DNA methylation and hydroxymethylation are highly aberrant in cancers, leading to abnormal gene expression and genomic instability, we will take the DNA methylation-demethylation cycles as a starting point of our research, with an emphasis on understanding the role of TET proteins in normal and oncogenic hematopoiesis.