More specifically, the IDO1-Kyn-AhR pathway has been shown to regulate the immune dormancy of tumour-repopulating cells treated with IFN-γ28, whereas the TDO2-Kyn-AhR axis has been demonstrated to play a critical role in protecting against anoikis in suspended breast cancer cells12 and in increasing glycolysis to drive APC-deficient colorectal cancer growth and recruiting macrophages into the tumour microenvironment to suppress immune surveillance22. The gene discussed is AHR; the disease is neoplasm.