In a similar study, analysis of WES of 25 BE/EAC pairs led to a model of two genomic trajectories of how BE transforms [43]: in trajectory 1, a gradual accumulation of alterations frequently affecting TP53, CDKN2A and SMAD4 leads to dysplasia and genomic instability, where, finally, oncogene amplification results in EAC. This evidence concerns the gene TP53 and Barrett esophagus.