The mechanism behind this synergistic antineoplastic effect lay in specifically arresting the cancer cell progression at G0–G1 phase, inducing the cell apoptosis via reactive oxygen species (ROS)‐dependent pathway, and mediating the cross‐action between PI3K/Akt (phosphatidylinositol 3‐kinase/protein kinase B) and JAK2/STAT3 (janus kinase 2 (JAK2)/signal transduction and activator of transcription 3) signaling pathways. The gene discussed is AKT1; the disease is cancer.