In summary, our study demonstrates that the mice whose p53 genes were specifically knocked out in the esophageal epithelium involve a multistage progression from simple hyperplasia, mild atypical dysplasia, moderate atypical dysplasia to severe atypical dysplasia under the induction of NMBA, which is similar to the pathological process of human precancerous lesions of ESCC. The gene discussed is TP53; the disease is esophageal squamous cell carcinoma.