PTEN and myeloid leukemia: This process is inevitably accompanied by alterations in epigenetic regulation [32, 33] When the m6A methyltransferase (METTL3) nucleotide modification is absent in HSCs, the effective translocations of PTEN (methylation), cellular-myelocytomatosis viral oncogene (c-Myc), and B-cell lymphoma-2 (BCL2) are downregulated, partially activating AKT, causing myeloid cells to differentiate towards a malignant phenotype and increasing apoptosis, providing a theoretical basis and direction for targeted therapy of myeloid leukemia [33].