Different cancers seem to have altered different key components of that mechanism, which may be connected with gene activity patterns in different target cells.6 The mechanism involves pRB and its immediate upstream regulators, the cyclin dependent kinases (CDK4 and CDK6), their catalytic partners (cyclin D1, cyclin D2 and cyclin D3), and the members of the INK4 family of CDK inhibitors (p16INK4a, p15INK4b, p18INK4c and p19INK4d). This evidence concerns the gene RB1 and cancer.