The esophageal disease, Eosinophilic Esophagitis (EoE) is a chronic and allergic disease. EoE is driven by food allergens which trigger Type 2 inflammation in the esophagus and causes symptoms such as vomiting, stomach pain, and difficulty swallowing. Increasing in prevalence, EoE poses a significant quality of life burden to patients. Left untreated, either due to diagnostic delay or ineffective treatments, EoE patients can develop fibrosis of the esophagus (FS-EoE) with worsening symptoms including food impaction and esophageal stricture. Histopathologic manifestations of the disease include basal zone hyperplasia, which worsens the barrier function of the epithelium. To date, there is no published research mechanistically linking fibrotic tissue stiffening to hyperproliferation in EoE. We sought to explore the molecular mechanisms of this hyperproliferation and fibrosis. In order to map hyperproliferation, we sought to use KRT14 as a marker of proliferative basal cells. To map epithelial cell differentiation, we sought to use KRT13 and KRT4 as markers of differentiated suprabasal cells. Esophageal biopsy from control and EoE patients were stained for basal and suprabasal cell markers, KRT14 and KRT13/KRT4, respectively. Here we have confirmed that KRT14 and KRT4 can be used to map the basal and suprabasal layers, respectively, in esophageal epithelium. In EoE epithelium, there is an expansion of the basal (KRT14+) and early suprabasal (KRT14- KRT13+KRT4- ) cell layers. While KRT14 has been assessed in EoE tissue, here, we quantified KRT14+ basal expansion on a protein level. Likewise, while sequencing has revealed increases in suprabasal cell markers, here, we have quantified KRT13 and KRT4 on a protein level. To understand epithelial cell differentiation in vitro, we confirmed that this stratification pattern was recapitulated in submerged and 3D ALI model systems, with KRT14 expressed in proliferative basal cells, and KRT4 expressed in differentiated, barrier-forming suprabasal cells. The promoters for KRT14 and KRT4 were therefore used to successfully drive expression of fluorescent proteins, DsRed and eGFP, respectively. In order to understand the relationship between fibrosis and hyperproliferation in FS-EoE, the proliferation-associated and mechano-sensing transcriptional co-factor, Yes-associated protein (YAP) was assessed for its role in esophageal epithelial cells and EoE. While YAP has been studied in muscle in EoE, here, for the first time, we investigate the role of YAP in non-FS- and FS-EoE tissue and in esophageal epithelial cells. We have found that YAP-mediated transcription is increased in EoE and further increased in FS-EoE tissue. We have found that YAP protein not excluded from nuclear localization in EoE tissue. YAP is not sequestered at cell-cell junctions, mirroring EoE-related barrier deficits. We found that in vitro, YAP cellular location is responsive to cell density and ECM stiffness in esophageal epithelial cells. Pharmacologic-induced nuclear YAP translocation, via XMU-MP-1 was seen to increase migration of EPC2-hTERT cells, in an EMT-like manner in submerged cultures. In air-liquid interface (ALI) cultures, pharmacologic upregulation of nuclear YAP is shown to decrease barrier function in an EMT-like manner and enriched the suprabasal cell population. Therefore, in EoE and FS-EoE, YAP signaling likely contributes to decreased barrier and fibrosis through EMT and to basal zone hyperplasia through maintenance of the KRT13+ cell population.