However, RT simultaneously trigger compensatory mechanisms that contribute to immunosuppression: (1) increasing PD-L1 expression on tumor cells and regulating the expression of multiple IC molecules on immune cells, thereby promoting tumor immune evasion and T-cell exhaustion; (2) enhancing regulatory T cells (Tregs), which suppress both adaptive and induced immune responses; and (3) inducing lymphopenia and immune cell depletion [25,26]. The gene discussed is CD274; the disease is neoplasm.