AKT1 and neoplasm: Since AhR plays differential or even opposing roles in tumorigenesis depending on its binding ligands3, 4, 5, the reduction of oncogenic factors (such as Akt-pS473 and Oct4-pT235) and the increase in tumour-suppressive factors (such as E-cadherin; Fig. 3c) indicated that ITE may specifically reduce the oncogenic pool of AhR while maintaining and activating the tumour-suppressive pool of AhR that transcriptionally repressed Oct4.