TGFB1 and eosinophilic esophagitis: TGF-β1 is released by several inflammation cells in the esophagus [16], and although it has involvement in wound healing, its continuous expression in EoE might act as a driver of pathologic remodeling, i.e., by increasing the fibroblast expression of herpes virus entry mediator (HVEM) [14], a receptor for LIGHT involved through the nuclear factor kappa B2 (NF-κB2) signaling pathway in pro-inflammatory and anti-homeostatic gene expression [17].