Furthermore, our finding that CDK2 inhibitor monotherapy exerts durable control of tumor growth in vivo in CCNE1-amplified cancers (associated with persistent Rb hypophosphorylation and a reduction in cyclin A2) signifies that CDK4/6 activity does not rapidly compensate for CDK2 inhibition to restore proliferation, in contrast to what has been reported in nonmalignant cells (18). Here, CDK4 is linked to neoplasm.