In the light of our findings, we posited a probable dependence of disease progression in patients with HCC on expression and/or activity aberrations in oncogene PDK1, which is reminiscent of oncogene addiction, such that the therapeutic targeting of PDK1 or selective blocking of its activities was enough and sufficient to suppress cell viability, impede proliferation, inhibit colony formation and deactivate the PI3K/AKT/mTOR signaling cascade. The gene discussed is MTOR; the disease is hepatocellular carcinoma.