The cyclin-dependent kinases form complexes with their cyclin partners and with CDK inhibitors. CDK6 and CDK4 associate with the D-type cyclins and target the retinoblastoma protein, allowing passage through the G1/S phase restriction point (1). CDK6/cyclin D complexes are sequestered in their inactive form through binding to one of the INK4 CDK inhibitor family members (2,3). Unlike the INK4 family of cdk inhibitors, the CDK inhibitor p21 Waf1/Cip1 may enhance the association of CDK4 and CDK6 with their cyclin D partners (4).