A number of potential anticancer agents that selectively modulate the activity of Cdk4-cyclin D1 in vitro have been reported.14 These molecules also show the genotypic consequences of Cdk4 enzyme inhibition at the cellular level, that is, growth inhibition of cancer cells in vitro, arrest of asynchronous cells at G0/G1 and prevention of pRb phosphorylation at Cdk4-specific serine residues.15, 16, 17 Usually, competing with ATP molecules for binding at the protein kinase active site is the normal mechanism by which most small molecules inhibit kinase enzyme activity. Here, CDK4 is linked to cancer.