Hence, we further studied the role of AKT as a downstream effector of CBX7 and found that treatment with PI3K/Akt inhibitor LY294002 could partially inhibit enhanced gastric cancer cell proliferation, migration and invasion, and ability of sphere formation induced by high expression of CBX7, while exogenous high expression of constitutively active AKT (mAKT) can reverse decreased gastric cancer cell proliferation, migration and invasion, and ability of sphere formation due to CBX7 interference. The gene discussed is AKT1; the disease is gastric cancer.