Persistent and weak STING/IFN‐I pathway cultivates the immunosuppressive tumor microenvironment by recruiting myeloid cells via CCR2.[91] Moreover, IFN‐I is implicated in upregulating the expression of immune checkpoints, such as PD‐L1, in tumor cells, increasing their resistance to immunotherapies.[92]. The gene discussed is CCR2; the disease is neoplasm.