Heterozygous deletions of the region on chromosome 18q containing SMAD2 and SMAD4 were present in approximately 30–70% of patients with precancerous BE [28] and in approximately 70% of oesophageal adenocarcinomas associated with BE [28,29], suggesting that such heterozygous deletions are early events in tumour transformation. Here, SMAD4 is linked to neoplasm.