In order to test this hypothesis, we selected a constitutively active (CA)-AhR-expressing transfection animal, because it was demonstrated that CA-AhR translocates into the nucleus and induces AhR target genes without ligands [37, 38] and that CA-AhR model animals manifest signs of dioxin toxicity, such as thymic involution, liver enlargement, and stomach cancer [39–41]. This evidence concerns the gene AHR and gastric cancer.