To further evaluate the molecular changes resulting from the effects of AP in HCC, we assessed the PI3K/AKT/mTOR pathway as a major intracellular signal transduction pathway involved in regulating the cell cycle, cell proliferation, apoptosis, metabolism, and angiogenesis The flow cytometry results indicated the elevated phosphorylation of PI3K, AKT, and mTOR in Hep3B were inhibited in a dose-dependent manner, following AP treatment (50 μg/mL, p < 0.05; 100 μg/mL, p < 0.01; Figures 3A–C). The gene discussed is MTOR; the disease is hepatocellular carcinoma.