By using the CUT&Tag profiling technique, we identified different sets of genes under these two scenarios: ADT-induced TDO2-Kyn-AhR signalling activated more apoptotic protective genes that promoted the survival of dormant cells and maintained their dormant state, whereas TDO2-Kyn-AhR signalling in recurrent CRPC activated more proliferative oncogenes to facilitate dormancy exit and aggressive growth of recurrent cancer cells (Fig. 5). This evidence concerns the gene AHR and cancer.