By manipulating CCND1 or/and NF-κB levels in lung cancer cells, we revealed that (1) overexpression of CCND1 resulted in cell proliferation and induced cell cycle arrest at the S phase; (2) overexpression of CCND1 promoted lung cancer progression and liver metastases; (3) Depletion of NF-κB and the following PI3K/AKT pathway in conjunction with CCND1 upregulation sufficed to reverse the oncogenic roles of CCND1. The gene discussed is AKT1; the disease is lung carcinoma.