Moreover, the immune evasion caused by the tumor microenvironment (TME) also causes a reduction in the therapeutic effect of ICB.[5] Therefore, a strategy that can promote the anti‐PD‐L1 therapy response while simultaneously alleviating the immunosuppression of TME would be valuable for improving the therapeutic efficacy of PD‐(L)1 blockade against TNBC. The gene discussed is CD274; the disease is neoplasm.