BE has been widely recognized as a premalignant lesion that can develop into EAC and published literatures have demonstrated that inflammation can significantly increase the risk and promote the establishment of BE from GERD,53,54 in which proinflammatory cytokines, such as IL-6,55 IL-8,56 IL-17,57 and TNF-α,58 may play a central role53,59 in promoting the progression of BE to EAC.52,60 Zhong et al.61 reported that the expression level of IL-4 in the tissues is increased in BE as compared with GERD and control, indicating an early upregulation of IL-4 in the premalignant stage. This evidence concerns the gene IL17A and gastroesophageal reflux disease.