TP53 and esophageal squamous cell carcinoma: According to these findings, a model of ESCC development was proposed implying that heterozygous TP53 mutations at the level of single cells in normal esophageal epitheliums confer a proliferative advantage, allowing for clonal expansion, and a population of these cells persisting over time may undergo LOH at the level of a normal TP53 allele; most cells with LOH are lost due to neutral competition, but few mutant clones persist over time and develop genome instability, acquiring CNAs, and may progress to form ESCC [19].