Mechanistically, persistent STAT1‐driven IFN‐γ signalling characterised high‐KIMA tumours, promoting immunosuppressive microenvironments enriched in regulatory T cells (FOXP3 and IL2RA), exhausted T cells (TIGIT and CD27) and immune evasion chemokines (CXCL10)7 (Figure S6). The gene discussed is TIGIT; the disease is neoplasm.