Ergo, the principle behind developing IDO1 inhibitors was two-fold; first to block IDO1 in tumor cells, which may be dependent on KYN production for 1-carbon units, NAD biosynthesis and other products of TRP, including KYN itself, which can bind to and activate the aryl hydrocarbon receptor (AHR) (Schmidt and Bradfield, 1996) and second, by inhibiting IDO1 activity in tumor-infiltrating myeloid cells. Here, AHR is linked to neoplasm.