Two primary mechanisms have been identified (1): Hyperactivation of METTL3 evokes AML cell proliferation and inhibits differentiation by promoting the translation of oncogenic targets such as c-MYC, BCL2, and PTEN (103); (2) CAATT enhancer binding protein Zeta (CEBPZ) recruits METTL3 to the transcription start site, leading to the enhanced translation of oncogenes SP1 and SP2 (104). Here, METTL3 is linked to acute myeloid leukemia.