The key role played by Cdk4–Cyclin D and Cdk6–Cyclin D in presiding over cellular proliferation, and the contrast between the ability of mice to survive genetic ablation of Cdk4, Cdk6 and Cyclin D and the addiction of cancer lines to these kinases, prompted the development of clinically successful Cdk4/6 inhibitors [62–66]. This evidence concerns the gene CDK4 and cancer.