In the in vitro study, the tumor-infiltrating CD11b+ macrophages could efficiently cross-present to tumor-infiltrating CD8+ T lymphocytes but they were unable to provide costimulatory signals, including CD80, CD86, and intercellular Adhesion Molecule 1 (ICAM-1), which caused the loss of killing ability by the CD8+ T lymphocytes [124]. The gene discussed is CD86; the disease is neoplasm.