The fact that sulfated glycoproteins (likely mucins; Figure S2) dynamically redistribute during metaplasia may explain why sulfated mucin expression is heterogeneous/variegated when viewed in chronic metaplasia in humans.20 Such metaplasia would be subject to chronic inflammation and repair in a non-synchronous fashion so that we might observe cells at various states of sulfated mucin trafficking, as has been reported by us and others in Barrett’s esophagus,24 intestinal metaplasia of the stomach,24,49 and pancreatic intraepithelial neoplasia 3.19,20. This evidence concerns the gene MUC5AC and esophageal adenocarcinoma.