Moreover, CWI1‐2, a small‐molecule compound, was recently identified to suppress IGF2BP2 and its functional targets (MYC, GPT2, and SLC1A5) and disrupt the Gln pathway, thereby attenuating the colony‐forming and self‐renewal abilities of AML cells, delaying the onset of leukemia, and prolonging the survival of mice with MA9‐induced leukemia. This evidence concerns the gene SLC1A5 and acute myeloid leukemia.