TET2 and myeloid neoplasm: They concluded that TET2 deficiency skewed differentiation of hematopoietic stem/progenitor cells, that TET2 can function as a driver in the pathogenesis of myeloid malignancies, but given the disease latency (one year) and low penetrance (20–30%), as in the human disease, cooperation with additional genetic lesions is necessary to cause the full-blown disease.