The above account illustrates how tumours establish suitable conditions for their growth and proliferation by increasing their uptake of tryptophan and ensuring an adequate supply of NAD+ and by simultaneously undermining host defences through a series of effects involving increased Kyn and KA, AhR activation, decreased NAD+ synthesis from Trp in the de novo pathway and up-regulating NAD+-consuming enzymes. The gene discussed is AHR; the disease is neoplasm.