Vitexin was found to abrogate hepatocellular carcinoma invasion and angiogenesis and induce hepatocellular carcinoma cell apoptosis through suppressing AKT/STAT3 signaling or activating JNK signaling [34–36], and it has been reported that vitexin inhibits proliferation and triggers apoptosis of glioblastoma, non-small-cell lung cancer, and renal cell carcinoma cells through suppressing the PI3K/Akt/mTOR signaling pathway [14, 37, 38]. The gene discussed is STAT3; the disease is glioblastoma.