Thus, we propose that one of the anti-tumor mechanisms of GBK treatment would somehow propagate the signal via a downstream substrate such as p53, which would in turn activate the transcription of the CDK inhibitor p27 and increase the binding of p27 to CDK2, suppress the activities of G1/S-CDK (cyclin E/CDK2), inhibit the phosphorylation of Rb protein, restrict the release of Rb from E2F, and lead to downregulation of MCM transcription and replicative arrest. This evidence concerns the gene CDK2 and neoplasm.