SOAT1 and neoplasm: This process contributes to local immunosuppression within the tumor microenvironment, facilitating the survival and escape of cancer cells.[15] IDO1 expression is typically induced by pro‐inflammatory cytokines such as interferon γ (IFN γ) and tumor necrosis factor‐α (TNF‐α) and is regulated by JAK/STAT and NF‐κB signaling pathways;[16] However, the mechanisms by which these pro‐inflammatory cytokines interact with other signaling pathways to collectively modulate the homeostasis of tryptophan metabolism remain unclear.