It is well known that CAFs are the major source of IL‐6 within the TME, where it has been implicated in contributing to tumor growth and metastasis.[40] Furthermore, the presence of IL‐6 in TME can polarize Mφ toward the M2 phenotype, implying the synergistic influence of tumor–stromal–immune crosstalk in aiding tumor progression.[33b] Another hallmark capability of cancer is to switch the energy metabolism. The gene discussed is IL6; the disease is neoplasm.