The strength of the L2-IL-1β transgenic mouse as a model of BE and progression to EAC is that it is 1) dependent upon chronic esophageal inflammation, 2) that the metaplasia, which mimics BE at the level of morphology and gene expression, occurs at the SCJ as it does in BE, and 3) that bile acids can both accelerate disease progression and enhance intestinalization. This evidence concerns the gene IL1B and Barrett esophagus.