CDK2 and neoplasm: Since CCNE1 was recurrently amplified, overexpressed, and often co-amplified with ERBB2 in our tumor samples, we took a special interest in druggable CDK2 whose activity is regulated by Cyclin E1 produced by CCNE1. The predicted response rate to existing CDK2 inhibitors was 29.8% (37/124) in all our patients and 24.7% (22/89) in our patients without ERBB2 amplifications, compared with 16.2% (17/105) and 15.3% (13/85) in TCGA ACGEJ patients, respectively.