This result was associated with the secretion of indole-3-carbaldehyde (I3A), a tryptophan catabolite, which activates tumor-infiltrating CD8+ T cells and improves their cytotoxicity via AhR signaling; ICB responses in a preclinical model of melanoma were only improved when tryptophan and Lactobacillus reuteri coexisted temporally and spatially, suggesting that I3A-driven tryptophan catabolism may reverse the pro-tumor effect of tryptophan [146]. The gene discussed is AHR; the disease is neoplasm.