In 2013, [11] demonstrated that miR-22 exerts proto-oncogenic activity in MDS and hematological malignancies by being strongly overexpressed and by negatively regulating TET2, a tumor-suppressor that is recurrently mutated or inactivated in a variety of human hematological tumors (i.e., MDS, myeloproliferative neoplasm (MPN), chronic myelomonocytic leukemia (CMMoL), and AML) [11,73,74,75,76]. The gene discussed is TET2; the disease is acute myeloid leukemia.