The results of molecular docking showed that the hub targets had good binding with fraxetin.<h4>Conclusion</h4>Fraxetin may inhibit AML cell proliferation and induce AML cell apoptosis through multiple targets, such as AKT1, SRC, and EGFR, and multiple pathways, such as focal adhesion and the PI3K-AKT signaling pathway. The gene discussed is AKT1; the disease is acute myeloid leukemia.