For instance, in a mouse model of colitis-associated tumors, colonic epithelial cell-specific deletion of the expression of AhR in the colon resulted in increased stem cell proliferation in the intestinal crypts, increased organoid-forming efficiency when colonocytes were cultured ex vivo, and led to a greater incidence and size of adenomas and adenocarcinomas [115]. This evidence concerns the gene AHR and adenocarcinoma.