Of note, the reduction extent of tumor volumes achieved by MIT/AREG mAb was slightly but significantly higher than that caused by either MIT/atezolizumab or MIT/nivolumab, not only underscoring the superior potential of classic chemotherapy combined with anti‐PD‐L1/PD‐1 agents in functionally competent TME, but also proving that the modality can be alternatively reconstituted by replacing PD‐L1/PD‐1 antibodies with an AREG mAb (Figure 6h). The gene discussed is PDCD1; the disease is neoplasm.