The implications of this are two-fold: first, it suggests that CDK2 inhibitor monotherapy (rather than combined CDK2/4/6 inhibition) should be the therapeutic strategy of choice for clinical trials in CCNE1-amplified tumors; second, it suggests that CDK2 inhibitors might have a wide therapeutic window in this setting, enforcing cell cycle arrest in tumor cells but not in other cells within the organism. This evidence concerns the gene CCNE1 and neoplasm.