Indeed, it has been demonstrated that the aberrant fusion protein RUNX1::RUNX1T1 was able to recruit a transcriptional repressor complex including DNA methyltransferase 1 (DNMT1) and histone deacetylases (HDACs), leading to chromatin remodeling, silencing of several genes involved in normal hematopoiesis and differentiation blockage in CBF-AML with t(8;21) [8, 9, 47]. The gene discussed is DNMT1; the disease is acute myeloid leukemia.