For instance, the m6A writer METTL3 has been found to be overexpressed in acute myeloid leukemia (AML) cell lines; it is considered to be accountable for the increased m6A methylation profiles and the translational activation of the MYC proto-oncogene, phosphatase and tensin homolog (PTEN), and the BCL2 apoptosis regulator mRNA transcripts, thus sustaining cell survival and proliferation [172]. Here, MYC is linked to acute myeloid leukemia.