In mRNA decay experiments, after actinomycin D treatment, the abundance of ATG5 mRNA in the CELF1 knockdown group decreased significantly over time compared to the control group, indicating that CELF1 specifically binds to ATG5 mRNA in AML cells and increases its half-life (Fig. 5C, D). The gene discussed is ATG5; the disease is acute myeloid leukemia.