CEACAM1 homophilic interactions and the CEACAM1 heterophilic interactions with CEACAM5 inhibit NK-mediated killing independently of major histocompatibility complex (MHC) class I recognition and also interfere with the interferon-γ (IFN-γ) release activities of NK cells, as well as tumor-infiltrating lymphocytes (TILs) [6, 41–43]. The gene discussed is CEACAM5; the disease is neoplasm.