In summary, we demonstrated that BHGJT efficiently inhibits tumor growth in vitro and in animal models and verified that BHGJT induced pronounced cell cycle arrest at the G0/G1 phase by downregulating CDK4 and Cyclin D1 and promoted apoptosis by a mitochondria-dependent pathway via AKT/GSK3β/β-catenin signaling. The gene discussed is AKT1; the disease is neoplasm.