found that MHC‐I expressed on tumor cells played a critical role in resisting macrophages‐mediated phagocytosis via the interaction of its B2M subunit with LILRB1 on macrophages.[216] Genetically blocking MHC‐I‐LILRB1 axis could elicit tumor‐phagocytosis of macrophages in vitro and in vivo. The gene discussed is B2M; the disease is neoplasm.