Describing the systems-level interactions between Cdk2, CyclinE, CyclinA, and CKI is also highly relevant to gaining insight into the dysregulated G1/S progression of cancer cells, where mutations and epigenetic events often conspire to increase CyclinE and downregulate p27Kip1 levels (Chu et al., 2008, Fero et al., 1996, Hershko, 2010, Kiyokawa et al., 1996, Nakayama et al., 1996, Scaltriti et al., 2011). The gene discussed is CDK2; the disease is cancer.