Adenocarcinomas of the esophagus and stomach are believed to originate from intestinal metaplasias that are triggered by inflammatory insult of the normal mucosa. Analysis of expression profile of samples representing these pathologies identified alterations in genes pertaining to glycerolipid and cytokine pathways. We identified augmented expression of proinflammatory signals as well as diminished expression of genes responsible for metabolism of lipid peroxides and aldehydes, known to induce DNA damage. Unbalanced expression of these genes could be, in part, responsible for oncogenic transformation during chronic inflammation. The figure represents the altered correlation of genes from glycerolipid pathways in Barrett's mucosa and adenocarcinomas of the gastroesophageal junction. For details, see the article by Gomes et al. on page 7127 of this issue.