In addition, novel tumour therapeutic agents (e.g., cuproptosis and DNA damage response inhibitors) are thought to recruit IFN‐γ‐, TNF‐α‐ and IL‐2‐secreting T cells to the TME by enhancing the activation of the cGAS–STING–IFN intrinsic immune pathway, which acts as an intermediary for T‐cell recruitment and remodelling of the immune‐suppressive metabolic state of tumour cells, such as IDO‐1‐mediated tryptophan degradation and dysregulated fatty acid metabolism.227, 228, 229. The gene discussed is TNF; the disease is neoplasm.