The expression of a variety of co-regulatory receptors on macrophages, such as PD-L1, PD-L2, CTLA-4 ligands B7-1 and B7-2, Tim-3, CD47, V-domain Ig suppressor of T cell activation (VISTA), and B7-H4 (16–18), has been shown to correlate with exhausted T cell phenotypes and therefore with an immunosuppressive tumor environment and poor clinical outcome (18–20). The gene discussed is CD86; the disease is neoplasm.