Though associated with changes in gut bacteria, a consistent microbial signature in patients has not been identified.298 The pathogenesis of CeD is known to primarily mediated by gluten-specific inflammatory Th1 and Th17 cells.299,300 Multiple studies have reported simultaneous expression of regulatory cytokines like IL-10 and TGF-β along with inflammatory cytokines IFN-γ, IL-17, and IL-21 in CeD.301–303 This creates a paradoxical environment in untreated CeD, where regulatory mechanisms attempt to suppress inflammation and mitigate the abnormal immune response triggered by gliadin.304. Here, TGFB1 is linked to cranioectodermal dysplasia.