Knocking down AhR by siRNA in LNCaP cells treated with ADT resulted in significant downregulation of the antiapoptotic genes BCL6, SHC3 and KRAS (Fig. 5e), suggesting that one of the primary roles of the TDO2-Kyn-AhR pathway, which is activated in early prostate cancer following ADT, is to prevent apoptosis, enabling cancer cells to survive and maintain themselves as dormant cells. This evidence concerns the gene KRAS and cancer.