Cyclin-dependent kinases (CDKs) are serine/threonine kinases that regulate cell cycle control and progression (1,2). A CDK holoenzyme complex is active if associated with its cyclin partner and if the complex is phosphorylated at specific activating residues (threonine 160/161; refs. 1 and 2). The progression through the cell cycle is mediated by the sequential activation of CDKs during different phases of the cycle. The G1/S phase transition of the cell cycle is mediated by phosphorylation of the Retinoblastoma gene product (Rb) by CDK4 and/or CDK6 (G1/ S checkpoint), leading to the release of bound E2F from Rb and allowing the transcription of genes by “free E2F” necessary for S-phase progression. During late G1 phase, the CDK2/cyclin E complex phosphorylates several substrates, including Rb. However, CDK2/cyclin A complex is active throughout the S phase. For cells to progress to mitosis, CDK1 (CDC2) must be “activated,” and activated cdc2 phosphorylates substrates required for mitosis (3).