Consistent with this experimental evidence for cdk independence of cyclin D1's role as a driver oncogene, human breast cancers overexpressing cyclin D1 do not show high levels of the canonical E2F target gene cyclin E [4, 5] and exhibit relatively normal proliferation rates compared to tumors with genetic deletion of pRb [4–6, 36]. This evidence concerns the gene RB1 and breast carcinoma.