A hypothetical chronological order of events in BE–EAC adenocarcinogenesis mediated by LIF may be as follows: LIF secreted by esophageal squamous and/or inflammatory cells in response to GERD, BE cells become LIF-dependent, GATA6-enriched dysplastic BE cells secrete high levels of LIF, LIF promotes the selection of M2 TAMs, M2 TAMs express high levels of immunosuppressive factors, and dysplastic BE cells progress to prometastatic EAC phenotypes as they evade immunosurveillance. The gene discussed is LIF; the disease is gastroesophageal reflux disease.