CDK2 and neoplasm: Expression of a constitutively active CCND1/CDK2 fusion protein results in RB hyperphosphorylation on sites preferred by CDK4 and CDK2, confers resistance to TGF-β induced growth arrest in MMTVD1-K2 mouse tumor cells, causes sequestration and inhibition of p21, and induces AIG in mink lung epithelial cells [22], [23].