In conclusion, the above evidence suggested a possible mechanism in CeD: the overexpression of IFN-γ by γδT cells acted on duodenal epithelial cells and upregulated expression of GSDMD through IRF1, transforming epithelial cells into “pre-pyroptotic” cell which was prone to pyroptosis under external stimulation. Here, IRF1 is linked to cranioectodermal dysplasia.