G1/S-phase checkpoint genes were disrupted, with CCND1 and CDK6 amplification as well as deletion of the CDK4/6 inhibitors CDKN2A and CDKN2B. Abnormal expression of CDKs and their partner cyclins is widely reported in esophageal cancer [61,62,63], and CCND1 amplification and nuclear expression have been shown to correlate negatively with survival [64,65]. Here, CDK4 is linked to esophageal cancer.