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. The gene discussed is RB1; the disease is neoplasm.