Perhaps the most salient difference between the mutational profiles in the majority of Barrett's stem cells representing cases that might never progress (for example, cases 4, 5, 6, 7, 8 and 9) to frank dysplasia and adenocarcinoma is the absence of both p53 mutations and amplified loci harbouring receptor tyrosine kinases (EGFR, c-MET, ERBB2, FGFR1, FGFR2) and other oncogenes such as KRAS, VEGFA, MDM2 and MYB)35, 36. This evidence concerns the gene MET and dysplasia.