Although such dysbiotic feature and its mechanistic link with celiac disease manifestation remain elusive, it is suspected that overgrowth of these pro-inflammatory endotoxin-secreting Gram-negative pathobionts may contribute to the gluten intolerance as well as the onset and/or progression of celiac disease, through the enhancement of the pro-inflammatory responses such as increased IFN-gamma and TNF-alpha production, which will impair gut barrier integrity and normal functioning. The gene discussed is IFNG; the disease is celiac disease.