Although most of the canonical mammalian Cdk-cyclin complexes have turned out to be dispensable for cell proliferation due to functional redundancy 57,58, cyclins and CDKs are found to be altered in a majority of human cancers (e.g., cyclin D1 is overexpressed in 25% of human mammary tumors), suggesting that they participate in different networks that control mammary tumor cell proliferation and growth. The gene discussed is CCND1; the disease is breast cancer.