As one of the most important tumor suppressors in hematologic malignancies (1–6), DNA methyltransferase enzyme DNMT3A is frequently mutated in myeloid neoplasms (MNs) as well as in their early precursors (7–9): its mutations occur in up to 36% of cytogenetically normal acute myeloid leukemia (CN-AML) patients, and 60% of clonal hematopoiesis of indeterminate potential (CHIP) (10, 11). This evidence concerns the gene DNMT3A and Melnick-Needles syndrome.