During the progression of GERD to EAC, IL-33, likely behaving as an alarmin responding to acidic insult, was unwaveringly elevated and localized into the cytoplasm of epithelial cells, from where it enacts its pro-proliferative effects and stimulates migration and invasion of tumor cells through ST2, while simultaneously inducing secretion of IL-6 [91] (Figure 4a). This evidence concerns the gene IL33 and gastroesophageal reflux disease.