The most successful approaches to impair tumor-elicited immunosuppressive mechanisms turned out to be monoclonal antibodies (referred to as immune checkpoint inhibitors) interfering with co-inhibitory molecules or their ligands, such as CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), PD-1 (programmed cell death protein 1), or PD-L1 (programmed death-ligand 1). The gene discussed is CD274; the disease is neoplasm.