In this study, by using high-purity C3G and a tumor xenograft model, it was demonstrated that C3G treatment could up-regulate KLF6 gene expression and KLF6 exhibited tumor growth–suppressing activity by cell cycle inhibition with a p53-independent up-regulation of p21 and disrupted the Cyclin D1 and CDK4 interaction. The gene discussed is KLF6; the disease is neoplasm.