The physical interaction between cancer-released CD200 and its inhibitory receptor (CD200R1) on APCs (Figure 1) suppresses secretion of pro-inflammatory cytokines, including interleukin 2 (IL2) and interferon gamma (IFNγ) [17,28] increases production of myeloid-derived suppressor cells (MDSCs) [10] and regulatory T-cells (Tregs) [29,30]; and compromises an anti-tumor immune response. The gene discussed is CD200; the disease is neoplasm.