In addition, METTL3 depletion in HSCs did not affect apoptosis (68), whereas knocking down of METTL14 induced acute myeloid leukemia (AML) cell apoptosis and promoted myeloid differentiation of normal HSCs via the SPI1–METTL14–MYB/MYC signaling axis (69). This evidence concerns the gene SPI1 and acute myeloid leukemia.