The interrelationship of cell cycle regulatory molecules in G1. Growth inhibitory and promoting signals impinge on the regulation of cyclin dependent kinase inhibitors (CKI). Growth promoting signals also directly lead to activation of cyclin dependent kinases (CDK) in G1. The cyclin dependent kinases serve to inactivate pocket proteins through phosphorylation leading to E2F transcriptional increases and cell cycle advancement. Cell cycle exit can be caused by activation of pocket proteins by phosphatases. In addition to blocking E2F transcription, recently activated pocket proteins also serve to negatively influence cyclin dependent kinase activity and positively influence CKI abundance. In this way, the regulatory molecules that control progression through G1 are extensively regulated by one another.