In the ESCC tumor microenvironment, modulation of AhR by using AhR activating ligand 3,3′-diindolylmethane decreased the levels of Vimentin and Slug along with reduction in the RhoA/ROCK1 signaling, which ultimately restricted COX2/PGE2 pathway, secretion of prostaglandin E2, EMT, cell migration and metastasis (35–37). This evidence concerns the gene AHR and neoplasm.