BCL2 and acute myeloid leukemia: Destruction of METTL3 reverses the arrest of bone marrow differentiation and growth loss, whereas overexpression of METTL3 promotes the proliferation in AML cells via a chromatin-based pathway to contribute to the translation of targeted oncogenes like c-MYC, BCL2, and PTEN, suggesting that METTL3 is an essential gene for AML growth (46, 47).