In vitro studies further showed that interleukin (IL)-13 [a cytokine with a central role in the pathogenesis of EoE, including recapitulating the esophageal transcriptome from EoE biopsy specimens [43]] reduces endothelial TSPAN12 expression, leading to an impaired barrier and elaboration of profibrotic mediators that ultimately increase ECM protein production by fibroblasts [42▪▪]. This evidence concerns the gene IL13 and eosinophilic esophagitis.