Moreover, we demonstrated that C-R tissues could increase the expression of Kyn, upregulate AhR (an endogenous ligand of Kyn [34]), which was dependent on TDO2 and AhR for anchorage apoptosis potential, we speculated that prostatic cancer cells utilized an autocrine signaling loop in which Kyn supported Abi and Dox resistance through an AhR dependent pathway, and the upregulation of TDO2 was central to this signaling loop. Here, AHR is linked to prostate carcinoma.