We have formulated a mathematical model for the G1/S regulation of the mammalian cell cycle. This mathematical model incorporates the key molecules and interactions that have been identified experimentally. By subdividing these critical molecules into modules we have been able to systematically analyze the contribution of each to G1/S dynamics. The primary module, which includes the interactions between cyclin E (CycE), cyclin-dependent kinase 2 (CDK2), and CDC25A, exhibits dynamics such as limit cycle, bistability, and excitable transient. The positive feedback between CycE and E2F causes bistability provided that the total E2F is constant and the retinoblastoma protein (Rb) can be hyperphosphorylated. The positive feedback between active CDK2 and cyclin-dependent kinase inhibitor (CKI) generates a limit cycle. When combined with the primary module, the E2F/Rb and CKI modules either potentiate or attenuate the dynamics generated by the primary module. In addition, we found that multisite phosphorylation of CDC25A, Rb, and CKI were critical for the generation of dynamics required for cell cycle progression.