The data from several studies supported this hypothesis owing to the fact that the DNMT3A-deficient model could develop lethal hematologic malignancies after the acquisition of cooperating mutations (Celik et al., 2015; Guryanova et al., 2016), and the overmethylation of CpG islands by DNMT3A may represent a residual trace of a failed attempt to limit proliferation and/or aberrant self-renewal (Miao et al., 2022). Here, DNMT3A is linked to hematologic disorder.