The main function of cyclin-dependent kinases (CDKs) is to regulate the process of cell cycle, and one of the important regulatory pathways is to block the cell cycle at G 1 phase by regulating Rb protein. CDK 4/6 can make Rb protein lose its blocking effect on cell cycle by phosphorylating Rb protein, and the activity of CDK 4/6 is affected by endogenous CDK inhibitors. It can be seen that there are three factors that may lead to cell proliferation in this pathway: over-expression of CDKs; The decrease of endogenous CDK inhibitors; Rb gene mutation. Theoretically, there are many strategies to treat tumors with these factors, but the focus of current research is to inhibit the activity of CDK subunits by acting on ATP sites of CDK. Two drugs with CDK inhibitor activity have entered the clinic, including flavopiridol and UCN-0 1. Flavopiridol induces cell cycle arrest in G 1 phase by inhibiting the activities of CDK2 and CDK4. In the recently completed phase I clinical trial, some effects were observed in 2 patients with renal cancer and 1 patient with non-Hodgkin's lymphoma. UCN-0 1 can eliminate G2 phase block, thus reducing the repair of DNA damage.