Interestingly, patients with mutator/MSI-type EGCs had a tendency to develop secondary metachronous cancer in the remnant stomach after initial ESD, which was statistically higher than the suppressor/p53 and unclassified type tumours (P<0.01, Figure 3A), whereas no correlation was found in the increase of metachronous gastric cancers by subclassification of tumours with mucin phenotypes (P=0.84, Figure 3B). This evidence concerns the gene TP53 and neoplasm.