This model has improved understanding of the potential cellular origin of BE in which researchers showed that BE can arise from gastric progenitors that are positive for Lgr5, and that IL-6 deficiency inhibited the development of BE and EAC suggesting a role for inflammation in inducing esophageal metaplasia and the progression of esophageal carcinogenesis (Quante et al., 2012). The gene discussed is LGR5; the disease is Barrett esophagus.