These data were also paralleled by the dysregulation of biological processes related to the transforming growth factor beta (TGFB), which was found to increase in the EoE by comparison with both the healthy and the GERD tissues (Fig. 3D and E), with specific markers distinguishing between EoE and GERD (Fig. 2E, specifically: WNT2, ACVRL1, POSTN, NOX4, LEFTY2, GDF5, and LTBP4), supporting the notion that the tissue remodeling and fibrotic process are associated with EoE pathogenesis [26]. This evidence concerns the gene LEFTY2 and gastroesophageal reflux disease.