Rosen et al reported that STAT6 activated in colon epithelial cells results in intestinal disorders and colitis, but they did not demonstrate whether STAT6 is related to epithelial cell hyperplasia.13 Our results demonstrate that STAT6 is responsible for TEC hyperplasia in GD, as hyperplastic TECs from both GD patients and EAGD mice highly expressed p-STAT6, and STAT6 deficiency reduced the disordered growth of TECs and rescued GD. Here, STAT6 is linked to intestinal disorder.