Our study confirmed that the main mutation type of TP53 in ESCC patients is a missense mutation, which may play a pivotal role in tumorigenesis because the p53 protein usually has positive expression, or even higher expression, owing to the accumulation of a nonfunctional protein that loss activity as a tumor suppressor, and some of which exert trans-dominant repression over the wild-type counterpart [31, 32]. The gene discussed is TP53; the disease is neoplasm.