(B) In response to mitogenic signals, CDKs become active and subsequently phosphorylate and inactivate pocket proteins, Cdh1 and CKIs. This generates positive autoamplification loops that render CDKs increasingly more active as the cell progress from G1/S towards mitosis. In fact, Cdk1 and Cdk2 will remain active from late G1 until anaphase. We propose to define this interval of time C phase, a phase with active Cdk1/Cdk2, as opposed to G0, early G1 and telophase that are characterized by no Cdk1/Cdk2 activity. However, CDKs also generate negative feedback signals that will induce their own inactivation in late M. CDKs not only phosphorylate downstream substrates to generate autoamplification loops, but they also generate negative feedback signals that will induce their own inactivation in late M. For example, Cdk1 promotes the activation of APC/CCdc20, both by phosphorylating certain subunits of APC/C and by inducing the degradation of Emi1. In turn active APC/CCdc20 causes the degradation of cyclins with the consequent inactivation of Cdk1. At the end of the cell cycle, CDC14 and other phosphatases (PPs) dephosphorylate many of the substrates phosphorylated by CDKs during the C phase. For additional detail see: D. Guardavaccaro and M. Pagano. Stabilizers and destabilizers controlling cell cycle oscillators. Mol Cell 22:1-4 2006.