The ability of cancer cells to subvert components of the host innate immune system and promote an inflammatory microenvironment favorable for cancer growth, including soluble factors that bind to myeloid cells [95], [96], [97], makes it conceivable that mannose receptor engagement by GPI anchors linked to tumor antigens such as mesothelin, folate receptor, CEA, and CaMOV18 [98], may represent another cancer strategy to escape immune surveillance [99]. The gene discussed is CEACAM5; the disease is cancer.