The progression from Barrett’s Oesophagus (BE), the only known precursor lesion from OAC, to invasive cancer is characterised by early chromosomal instability, probably due to p53 loss, often including genome doubling and a high frequency of chromothripsis events resulting in considerable genetic diversity followed by a later acquisition of driver mutations at sub-clonal frequencies3, 4, 5. Here, TP53 is linked to Barrett esophagus.