CEACAM5 and neoplasm: Notably, FcγRI‐CAR‐HMs within the tumor exhibited a CD86highCD206low phenotype, suggesting that CEA‐mediated FcγRI signaling effectively maintains the pro‐inflammatory M1 phenotype of CAR‐macrophages, even under the immunosuppressive pressures of the TME (Figure 5h; Figure S11d, Supporting Information).