Novikov et al. (2016) investigated the role of TRP-derived metabolites within malignant and non-malignant breast cancer cell lines and showed that (1) cell lines that expressed TDO produced sufficient intracellular KYN and XA concentrations to activate the AhR; (2) TDO overexpression led to excess KYN and XA, which accelerated the migration of tumour cells in an AhR-dependent manner; and (3) the environmental ligands TCDD and BaP, as well as the endogenous TRP-derivative FICZ mimic this effect [182]. The gene discussed is AHR; the disease is neoplasm.