Consistent with these findings, overexpression of the calpain-14 protein in esophageal epithelial cells leads to morphological changes and barrier defects independently of IL-13-mediated inflammation, while CAPN14 gene silencing in these cells leads to defects in barrier repair after IL-13 stimulation (Davis et al. 2016), suggesting that calpain-14 might contribute to EoE via a regulatory loop (Litosh et al. 2017). The gene discussed is IL13; the disease is eosinophilic esophagitis.