Although the same TDO2-Kyn-AhR pathway mediates both the protection of ADT-induced dormant cell death for androgen-dependent prostate cancer and the promotion of prostate cancer progression for recurrent CRPC, we assume that the setting for AhR activation is different and thus may activate the expression of different sets of genes under these two scenarios to allow for tumour dormancy and recurrence progression. This evidence concerns the gene AHR and Familial prostate cancer.