CDKN2A and Barrett esophagus: 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.