Clonal evolution is a fundamental process in the development of t-MDS and t-AML (12, 13); the proliferation of clones with pre-leukemic founder mutations in epigenetic regulating genes, such as the DNA methyltransferase 3A gene DNMT3A, tet oncogene family member 2 gene TET2, and additional sex combs-like 1 gene ASXL1, due to the accumulation of additional mutations or selection of resistant clones, is a well-recognized mechanism in the development and relapse of hematological malignancies (14, 15). The gene discussed is DNMT3A; the disease is acute myeloid leukemia.