Although mouse models of colitis are not directly comparable to human presentations of functional disease, given the TNF and IL-1β inflammatory profile in a subset of FD patients, a dysregulation in HIF transcriptional pathways, specifically in the form of a downregulation in HIF-1α, may provide a possible explanation for eosinophil recruitment and barrier dysfunction in FD pathophysiology. This evidence concerns the gene HIF1A and Fabry disease.