The molecular progression of GERD-BE-EAC is a complex process involving multiple genetic alterations, including chromosomal aberrations, allelic imbalance, microsatellite instability, methylated DNA, and microRNA alteration causing consecutive deregulations of their products, cell cycle regulatory factors, the loss of heterozygosity (LOH) in locus 9p21 (involving gene CDKN2A) and locus 17p13 (TP53), the increase in c-Myc, the up-regulation of minichromosome maintenance 2 (MCM2) and cyclin D1, and reduced cell adhesion molecules [5,8,9,11,42,43,44]. This evidence concerns the gene TP53 and Barrett esophagus.