CAR macrophages (CAR-M) can phagocyte tumor cells expressing a target antigen. It is herein shown that the proprotein convertase furin is over-expressed in human primary macrophages in the presence of tumor cells, which is a way to redirect these macrophages towards an anti-inflammatory phenotype. Conversely, inhibition of furin leads to the maintenance of their pro-inflammatory phenotype, even in a tumor cell environment. The present invention proposes to use furin-inhibited CAR-M derived from primary blood monocytes as a therapeutic strategy to treat solid tumors. Surprisingly, the generated furin-inhibited CAR-M display enhanced anti-tumor phagocytic activity against breast cancer cell lines and breast cancer patient-derived tumoroids and a persistent pro-inflammatory phenotype compared to furin-expressing CAR-M. Moreover, it was found that furin-inhibited CAR-M secreted factors can enhance T-cell proliferation and can thereby modulate the tumor microenvironment. Furin-inhibited CAR-M therefore represent a second-generation CAR-M therapeutic strategy for solid tumors.