KYNA originates from dietary tryptophan via the indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) pathways, which can be activated by both host immune cells and gut microbes such as Pseudomonas fluorescens and Lactobacillus spp. KYNA acts via the aryl hydrocarbon receptor (AhR) to promote Treg expansion and suppress cytotoxic T cell activity, contributing to immune escape in melanoma (30, 31). Here, AHR is linked to melanoma.