Correspondingly, IHC staining and western blotting showed that the lung metastases from MDA-MB-468/RGCC tumor-bearing mice existed a significant activation of AMPK compared with the lung metastases from control mice; Volasertib or Dorsomorphin treatment of MDA-MB-468/RGCC tumor mice dramatically reduced the activity of AMPK in the lung metastasis, whereas simultaneous O304 and Volasertib treatment of MDA-MB-468/RGCC tumor mice partially restored the activity of AMPK in the lung metastasis (Fig. 6E-F). This evidence concerns the gene PRKAA2 and neoplasm.