In conclusion, this work elucidated that depletion of circHIPK3 repressed proliferation, migration, and glycolysis and contributed to apoptosis of lung cancer cells in vitro, as well as blocked tumor growth in vivo, at least in part, by absorbing miR-381-3p and modulating the AKT/mTOR signaling pathway, affording a potential therapeutic molecular target for lung cancer. The gene discussed is AKT1; the disease is lung carcinoma.