Emerging evidence suggests a complex interplay between TGF‐β and STING signaling in the context of tumor progression.[25] For example, TGF‐β can negatively regulate STING expression and activity, impairing the STING‐mediated anti‐tumor immune response.[25] Conversely, STING activation can counteract the immunosuppressive effects of TGF‐β, thereby enhancing the efficacy of anti‐tumor immune responses.[26] However, several clinical trials utilizing STING agonists have not been successful,[27, 28] and the underlying mechanisms behind these failures remain unclear. This evidence concerns the gene TGFB1 and neoplasm.