Therefore, TP53 mutations, which disrupt cell cycle check points at the G1/S and G2/M transitions, and the amplification of an oncogene (CCND1) or the deletion of suppressor genes (CDKN2A/2B) strongly suggest that the disruption of G1 control is a key event in the development of ESCC (Figure 4). This evidence concerns the gene CDKN2A and esophageal squamous cell carcinoma.